Taufon thiab emoxipin tib lub sijhawm muaj ntshav qab zib

Feem ntau, ntshav qab zib yog nrog ib tug mob txaus ntshai xws li retinopathy. Kho tus kab mob qhov muag no raws li lub zog ntawm cov cuab yeej kho mob "Emoksipin." Nws yog dav siv nyob rau hauv kev xyaum ophthalmic, vim nws cov nyhuv kho, uas yog tsom rau qeeb ntawm qhov muaj mob ntawm kev puas tsuaj rau cov hlab ntsha qhov muag. Cov neeg muaj ntshav qab zib mellitus raug tso cai siv "Emoksipin" nruj me ntsis rau lawv lub hom phiaj thiab tom qab sab laj nrog tus kws tshaj lij.

TSEEM CEEB YUAV TSUM! Txawm tias cov ntshav qab zib siab tshaj plaws tuaj yeem kho tau hauv tsev, tsis tas yuav phais lossis tsev kho mob. Tsuas nyeem dab tsi Marina Vladimirovna hais. nyeem cov lus pom zoo.

Cov ntaub ntawv dav dav

Kev npaj tshuaj "Emoxipin" muaj ib tug xov tooj ntawm cov khoom muaj txiaj ntsig rau tib neeg. Nws ua kom lub cev tiv thaiv cov pa oxygen tsis zoo, tiv thaiv oxidation kev ua haujlwm thiab, vim li ntawd, tiv thaiv kev puas tsuaj rau cov kab mob me me thiab loj heev. "Emoksipin" siv kev koom tes hauv kev muab cov hlab ntsha nrog elasticity, lub zog thiab smoothness. Ua tsaug rau cov tshuaj no, txhawm rau kho cov ntshav hauv lub cev.

Qab zib yog txo tam sim ntawd! Mob ntshav qab zib ntev mus ntev tuaj yeem ua rau tag nrho cov kab mob, xws li teeb meem tsis pom kev, tawv nqaij thiab plaub hau, mob rau sab hauv, mob caj pas thiab mob qog nqaij hlav! Cov neeg qhia kev iab kev xav mus li qub rau lawv qab zib. nyeem rau.

Nws muaj "Emoksipin" tshaj tawm antithrombotic cov cuab yeej, uas muaj nyob rau hauv resorption ntawm cov ntshav txhaws. Tsis tas li ntawd, nws txoj kev siv txo qis transmittance ntawm lub vascular phab ntsa ntawm cov khoom ntawm lub zeem muag, tiv thaiv hemorrhage (ntshav ntws los ntawm lub nkoj tawg rau hauv lub cev) thiab myocardial atherosclerosis cuam tshuam.

Kev Sib Sau thiab daim ntawv ntawm kev tso tawm

Kev npaj tshuaj muaj peev xwm pom tau hais tias kev daws tshuaj rau kev txhaj tshuaj thiab tee npaj rau instillation ntawm lub qhov muag. Cov tshuaj tseem ceeb hauv cov tshuaj muaj pes tsawg leeg yog methyl ethyl pyridinol hydrochloride. Nws muaj lwm yam ntxiv Cheebtsam:

• txhaj dej
• sodium sulfite,
• phosphoric acid poov tshuaj ntsev,
• zaub mov ntxiv E211.

Tus sawv cev kws tshuaj "Emoksipin" yog tshaj tawm rau kev kho mob ntawm kev mob hauv qab no:

Ncos tau raug txiav txim siab nrog qhov tso siab hnyav ntxiv.

• kev puas tsuaj rau cov kab mob retina ntawm cov khoom hauv lub zeem muag tiv thaiv keeb kwm yav dhau los ntawm kev txhim kho ntshav qab zib,
• siab intraocular,
• cov nyom ntawm myopia,
• tshuaj lom neeg thiab huab cua kub heev rau ntawm lub qhov muag,
• intraocular hemorrhages ntawm ntau yam etiologies.

Yuav thov li cas?

Hauv nqe lus piav qhia rau cov tshuaj nws tau qhia tias nws yuav tsum siv ob zaug los yog peb zaug ib hnub, tso cov tshuaj 1-2 ib ce tso rau hauv txhua qhov muag. Cov no yog cov koob tshuaj pom zoo, thiab tus kws kho mob tsim tau ntau qhov tseeb dua ib tus zuj zus rau txhua tus neeg mob raws lub hnub nyoog, kev kuaj mob thiab cov nyom ntawm cov chav kawm ntawm tus kab mob. Lub sijhawm ntawm kev kho kom zoo yuav txawv los ntawm 3-5 hnub mus rau ib hlis. Emoxipin yuav tsum tau siv rau cov neeg mob ntshav qab zib mellitus, ua raws li qee txoj cai uas yuav pab ua kom tau qhov txiaj ntsig zoo tshaj plaws los ntawm kev kho mob thiab txo qhov kev pheej hmoo kis mob rau hauv thaj chaw muag. Cov kab ke ntawm kev coj ua yog raws li hauv qab no:

1. Siv xab npum ntxuav tes thiab so lawv qhuav.
2. Sawv ntsug nyob sab xub ntiag ntawm daim iav kom pom tias lub raj mis ze npaum li cas rau lub qhov muag.
3. Pov rov qab rau koj lub taub hau me ntsis, maj mam rub rov qab rau sab nraub qaum, saib sab thiab nqus dej ntawm cov tshuaj uas xav tau. Tsis txhob thawb daim tawv nqaij ntau dhau, vim tias cov tee dej tawm tuaj yeem tuaj yeem.
4. Nws tsis tas yuav txo qis lub raj mis dhau, vim tias koj tuaj yeem ua kev puas tsuaj rau lub qhov muag lossis nqa kab mob mus rau hauv nws los ntawm lwm qhov khoom nruab nrog ntawm lub zeem muag.
5. Tom qab instillation, tam sim ntawd kaw koj lub qhov muag thiab maj mam nias nrog koj tus ntiv tes los tiv thaiv qhov kev daws los ntawm nchuav.
6. Yog tias koj xav tau tso lub qhov muag iav, koj yuav tsum tos txog 1/3 teev tom qab kev tsa tawm.

Cov Yuav Tsum Muaj

"Emoksipin" yog suav tias muaj kev nyab xeeb heev rau tib neeg lub cev, yog li ntawd, nws tau siv tsis muaj kev txwv rau kev nkag. Qhov tsis txaus ntseeg tsis zoo rau txoj kev siv ntawm cov tshuaj tau piav yog hypersensitivity rau lub Cheebtsam ntawm nws muaj pes tsawg leeg. Tsis txhob siv "Emoksipin" thiab lub sijhawm thaum siv cev xeeb tub.

Phiv Txheej Xwm

Thaum siv Emoxipin, feem ntau yog thaum cov tshuaj tua kab mob ua txhaum cai, cov tsos mob hauv qab no yuav tshwm sim:

• liab ntawm lub qhov muag
• mob taub hau
• pom kev pom
• ntshav siab
• lacrimation thiab tingling,
• tsaug zog
• o rau thaj chaw muag,
• qhov hnov ​​ntawm hlawv.

Feem ntau, qhov tshwm sim tsis zoo tshwm sim hauv cov neeg mob uas muaj cov kab kev cov nyom uas yuav tsum muaj kev pab txhawb nqa kho mob niaj hnub. Feem ntau, cov kev mob tshwm sim sai daws nws tus kheej thiab tsis tas yuav muaj kev cuam tshuam ntxiv, tab sis yog tias qhov xwm txheej tsis nyob tus yees ntev, kev pab kho mob pom zoo rau tus neeg raug mob.

Cov lus qhia tshwj xeeb "Emoksipina" muaj ntshav qab zib

"Emoksipin", siv nyob rau hauv ntshav qab zib mellitus rau kev kho mob ntawm qhov muag kab mob, tsis pom zoo rau siv nrog lwm cov tee. Cov neeg mob uas siv cov lo ntsiab muag yuav tsum tau tshem tawm lawv ua ntej kev ua tiav. Lub raj mis tom qab qhib yuav tsum muab cia rau qhov txias. Cov chaw tsim khoom ntawm cov tee "Emoksipin" tau lees tias cov dej ua kom zoo txaus nws cov txiaj ntsig zoo rau 2 xyoos. Tom qab lub sijhawm no, kev siv cov tshuaj yog nruj me ntsis contraindicated.

Cov nqe lus ntawm kev muag khoom thiab kev cia khoom

Koj tuaj yeem yuav "Emoksipin" hauv lub tsev muag tshuaj, tab sis tsuas yog daim ntawv yuav tshuaj. Tom qab tau, nws yog ib qho tseem ceeb kom soj ntsuam cov kev mob cia ntawm cov tshuaj. Ncos tau khaws cia rau hauv qhov chaw tiv thaiv los ntawm lub hnub ci, ntawm qhov ntsuas kub tsis tshaj 24 degrees Celsius. Cov tshuaj tov yuav tsum muab cia rau hauv qhov chaw tsaus nti kom tsis ncav cuag rau cov menyuam yaus. Lub txee lub neej ntawm cov tee yog 2 xyoos, kev daws yog 3 xyoos.

Mob angiopathy mob ntshav qab zib tshwm li cas thiab nws yuav kho li cas?

Txog kev kho mob pob qij txha, peb cov neeg nyeem tau siv DiabeNot siv tau zoo. Pom qhov nrov ntawm cov khoom no, peb tau txiav txim siab muab nws rau koj kom txaus siab.

Cov teeb meem ntshav qab zib hauv ntiaj teb no tseem txhais tau tias yog kev kho mob thiab kev sib raug zoo, nws thiaj li muaj thoob plaws. Ntawm tag nrho cov kab mob endocrine, mob ntshav qab zib muaj txog 70%, thiab thoob ntiaj teb muaj kwv yees li 120-150 lab tus tib neeg cuam tshuam los ntawm tus kab mob no. Tab sis tsis tsuas yog tus kab mob nws tus kheej nqa tib neeg kev txom nyem. Ntau yam teeb meem txaus ntshai heev. Thiab ib qho ntawm cov qauv tshaj plaws rau tib neeg yog mob ntshav qab zib angiopathy - kev puas tsuaj rau cov hlab ntsha.

Nrog rau cov ntshav qab zib, mob ntsws ua rau lub hauv paus ua ntej ntawm kev puas tsuaj rau cov kabmob tseem ceeb ntawm ib tug neeg, thiab yog li ntawd ua rau muaj kev tsis taus. Ua ntej tshaj plaws, cov hlab ntsha cuam tshuam, pib nrog capillaries. Qhov phom sij tshaj plaws rau ntshav qab zib yog kev puas tsuaj:

• raum
• ceg qis dua
• tshuaj retina.

Mob taw: mob

Qhov tshwm sim uas ib txwm muaj nyob hauv ntshav qab zib yog ntshav qab zib txhawm plhuav angiopathy. Lub ntsiab lus ntawm tus kab mob no yog qhov poob ntawm bandwidth los ntawm capillaries, uas ua rau muaj kev ua txhaum nyob rau hauv cov ntaub so ntswg ntawm tus taw ntawm cov ntshav ncig, uas ua rau lawv atrophy. Angiopathy ntawm sab hauv qis dua tau ua raws li hauv qab no: ua ntej tus ntiv tes atrophy, tom qab ntawd txhais ko taw, ceg qis dua, thiab ncej puab. Atrophied qauv hloov pauv kev txiav tawm, raws li kev ua haujlwm gangrene pib tsim tawm.Hauv qhov xwm txheej no, kev hloov kho txuas ntxiv mus txuas ntxiv hauv cov ceg ntawm cov hlab ntsha.

Cov neeg mob uas cuam tshuam los ntawm hom tshuaj insulin-mob ntshav qab zib mellitus yuav tsum ua tib zoo xav txog thawj qhov tshwm sim ntawm tus kab mob.

Mob taw ntawm tus kab mob thaum pib tuaj yeem hais tawm:

• loog thiab txias ntawm tus taw,
• qaug dab peg
• ua txhaum ntawm kev rhiab
• nquag mob hauv txhais ceg
• ntev li ntawm dryness ntawm daim tawv nqaij ntawm ob txhais ceg,
• qhov kev hnov ​​mob hlawv
• tuab ntawm cov ntsia hlau.

Ntawm cov theem tom ntej, mob ncauj plab, ncauj tawv nqaij tas li ntxiv rau cov tsos mob no. Ntxiv mus, nws tsis yooj yim sua kom ncua kev kho mob, nws yog ib qhov tsim nyog yuav tau siv ntsuas kev kub ntxhov.

Cov tshuaj niaj hnub pom qhov txawv plaub ntu thaum tsim kho tus mob ko taw.

1. Hyperemia nrog edema ntawm ko taw.
2. Mob ntshav taw hauv theem ob yog nrog los ntawm kev hloov me me hauv cov pob txha, qhov pib deformation ntawm tus taw.
3. Nyob rau theem thib peb, qhov deformation ntawm lub taw yuav tsum tshaj tawm, qhov tshwm sim ntawm qhov kev tawg, cuam tshuam ntawm qhov qis qis ntxiv.
4. Ntawm qhov kawg, feem ntau txaus ntshai theem, diabetic ko taw kis tus mob txhab trophic, uas tom qab ntawd coj mus rau kev ua laib.

Kev kho mob ntawm angiopathy ntawm qis qis txhawm

Kev kho mob kho mob nqa txoj kev kho tsuas yog mus txog ib qho ntsiab lus, yog li ntawd, nws yog qhov yuav tsum tau nrhiav kev pab ntawm kws kho mob vascular sai li sai tau. Hmoov tsis zoo, thaum muaj kev ncua yam tsis tsim nyog, lub d taw ua ntshav qab zib ua rau txoj kev loj hlob ntawm tus mob caj dab, thiab txoj kev txum tim rov qab los ua ntshav tsis yooj yim sua.

Nyob ntawm theem thiab qib ntawm kev puas tsuaj rau cov hlab ntsha los ntawm angiopathy ntawm ko taw, qhov tsim nyog ntawm kev kho tus mob yog xaiv.

• Yog hais tias qhov ua rau mob ntshav qab zib ko taw mob siab rau kev cuam tshuam ntawm cov hlab ntsha tseem ceeb, ces lub luag haujlwm tseem ceeb yog kho ntshav ntws hauv cov ceg. Hauv qhov no, kev kho ntawm trophic mob ntawm taw yog ua tau. Txhawm rau kom ntshav ntws rov qab, txoj haujlwm ntawm leeg ntshav lossis kev cuam tshuam tsawg kawg yog kev ua haujlwm.
• Nyob rau hauv cov ntaub ntawv ntawm segmented nqaim ntawm cov leeg, cov txiaj ntsig zoo tau tiav los ntawm kev cuam tshuam endovascular.
• Yog tias angiopathy ua rau txhaws ntau ntxiv ntawm cov hlab ntsha, txoj haujlwm yuav hla mus. Nws muaj nyob rau hauv tsim cov khoom cua ntshav txaus.

Nrog rau ib qho twg, tus kab mob nyuaj tshaj plaws, lub ntsiab yog tsis txaus siab, tsis txhob tso. Nws yog ib qho tsim nyog los xaiv txoj kev kho kom raug thiab txuas ntxiv ua nws lub hom phiaj thiab txheej txheem.

Kuaj ntshav qab zib taw

Txhawm rau kom txo qhov zoo li ntawm qhov tsis txaus ntseeg no, nws yog qhov yuav tsum tau soj ntsuam tus kws kho qhov muag endocrinologist thiab ua qhov kev soj ntsuam txhua xyoo siv ultrasound scanning (ultrasound duplex scanning). Yog tias muaj mob thaum taug kev hauv qab ceg lossis ko taw, cov tsos ntawm trophic mob rau ntawm ko taw, necrosis ntawm daim tawv nqaij lossis ntiv tes, nws yog qhov tsim nyog los ua ultrasonic duplex kev soj ntsuam ntawm cov hlab ntsha ntawm sab hauv qis kom sai li sai tau.

Mob ntsws yog dabtsi?

Hloov pauv ntawm cov hlab ntshav tshwm sim los ntawm kev tsis sib haum xeeb hauv txoj cai ntawm lub suab nrov ntawm lawv cov laus yog hu ua retinal angiopathy. Angiopathy yog qhov muaj txiaj ntsig ntawm cov kab mob ntawm cov hlab ntsha ntawm lub cev, nrog rau cov hlab ntsha ntawm cov kab mob retina, uas ua rau cov zaub mov tsis haum ntawm lub cev khoom noj thiab ua haujlwm. Qhov no ua rau retinal dystrophy, ua rau txoj kev txhim kho ntawm myopia, qhov muag plooj.

Angiopathy yog qhov txawv txav los ntawm qhov hloov ntawm lub lumen lossis chav kawm ntawm cov hlab ntsha: lawv tau ntuag, nqaim, ua kom tiav, muaj ntshav puv, thiab lwm yam, uas nyob ntawm qhov laj thawj uas ua rau qhov kev hloov no. Feem ntau tus kab mob no loj hlob ntawm ob lub qhov muag tib lub sijhawm.

Hom mob angiopathy rau ntawm qhov retina:

1. Retinal hypotonic angiopathy qhia los ntawm kev nthuav dav ntawm cov hlab ntsha, txoj hlab ntshav txawv. Hlab ntsha hauv sab nraud zoo li crimped.
2. Cov kev mob ntshav siab (angiopathy) yog tshwm sim los ntawm kev kub siab. Nyob rau theem pib ntawm tus kabmob, tom qab tshem tawm qhov ua rau (kub siab), lub fundus tau txais kev nyob nyab xeeb.
3. Mob puas siab ntsws angiopathy tuaj yeem tshwm sim ntawm lub hauv siab ceev ceev ntawm lub hauv siab, raug mob rau lub hlwb, lub ncauj tsev menyuam caj dab, uas yog nrog los ntawm cov hlab ntsha zaws thiab nce siab intracranial.
4. Ntshav qab zib angiopathy ntawm lub qhov muag tuaj yeem tshwm sim nrog kev kho mob ntshav qab zib yam tsis raug mob. Nws muaj ob hom:

• microangiopathy - muaj nyob rau hauv cov phab ntsa hauv cov hlab ntsha me, tuaj yeem ua rau cuam tshuam hauv cov ntshav ncig, cov ntshav ntawm cov nqaij nyob ze,
• macroangiopathy - muaj nyob hauv yeej ntawm cov hlab ntsha loj dua ntawm cov retina.

Hauv kev mob ntshav qab zib angiopathy, cov phab ntsa ntawm cov hlab ntsha tau da dej nrog mucopolysaccharides, thiab cov xovtooj ntawm phab ntsa tuab. Qhov khoob ntawm capillaries nqaim, uas yav tom ntej tuaj yeem ua rau lawv kev txhaws tag. Cov kab mob no ua rau cov ntshav hla mus, uas tuaj yeem ua rau oxygen oxygen tshaib plab ntawm cov ntaub so ntswg. Nyob rau hauv qhov teeb meem feem ntau nyuaj, ntau txoj kev mob qog tuaj yeem ua tau, thiab vim li ntawd, qhov txo qhov tsis pom kev zoo.

Txoj Kev Kho Mob Rov Ntsia Kev Mob Hlwb

Retinal angiopathy yuav tsum kuaj los ntawm tus kws paub hauj lwm zoo. Tsuas yog ib tus kws kho mob tuaj yeem kuaj pom tus kab mob thiab sau ntawv yuav tsum tau kho. Feem ntau cov tshuaj yog kws kho mob uas ua rau kev txhim kho ntshav microcirculation hauv cov hlab ntsha ntawm qhov retina:

Rau kev ua tiav zoo rau kev mob ntshav qab zib angiopathy, ntxiv rau cov tshuaj, tus kws kho mob tau sau ib qho khoom noj tshwj xeeb uas tsis suav nrog cov khoom noj uas muaj cov khoom noj uas yog carbohydrate hauv cov zaub mov noj. Cov neeg mob uas kuaj tau kab mob ntshav qab zib angiopathy pom zoo ua kom lub cev qoj ib ce uas ua rau cov leeg noj qab zib thiab txhim kho cov hlab plawv.

Kev siv lub cev ua haujlwm ntawm kev kho mob (kho mob, kho hluav taws xob, kho laser, lub ntsej muag tsis haum) muaj cov txiaj ntsig zoo rau kev mob ntawm cov neeg mob zoo li no.

Yog li, hauv kev kho mob ntawm retinal angiopathy, lub luag haujlwm tseem ceeb rau ob tus kws kho mob tshwj xeeb thiab cov kws tshaj lij hauv cov liaj teb uas muaj feem cuam tshuam. Tus kws kho mob ntsej muag tuaj yeem hais kom siv cov vascular npaj Taufon, Emoksipin, cov vitamins qhov muag hauv daim ntawv ntawm cov ntsiav tshuaj (Anthocyan Forte, Lutein Complex) rau tus neeg mob. Lawv txhim kho txoj kev ntawm cov ntshav ncaj qha rau hauv cov hlab qhov muag thiab pab txhawb kev tiv thaiv ntawm tus neeg mob lub zeem muag, muaj cov nyhuv ntawm lub cev.

Cov tsom iav Sidorenko tau muaj pov thawj lawv tus kheej los ua lub tshuab ua kom lub hlwb zoo tshaj plaws uas tus neeg mob tuaj yeem siv ntawm nws tus kheej hauv tsev txhim kho kev mob ntawm nws lub qhov muag. Kev sib txuas ua ke pneumomassage, infrasound, phonophoresis thiab kev kho xim, lawv tso cai rau koj kom ua tiav cov txiaj ntsig hauv kev sib nrug luv. Kev ua haujlwm siab, kev nyab xeeb ntawm lub cuab yeej yog ua pov thawj los ntawm kev sim hauv chaw kuaj mob.

Ncos rau qhov muag nrog ntshav qab zib: cov cai ntawm kev siv, daim ntawv teev cov tshuaj noj

Tau ntau xyoo tsis muaj kev vam meej nrog DIABETES?

Lub taub hau ntawm lub koom haum: “Koj yuav xav tsis thoob tias yoojyim kho mob ntshav qab zib li cas los ntawm kev noj tshuaj txhua hnub.

Ib qho teeb meem ntawm cov ntshav qab zib yog kev puas tsuaj rau cov cuab yeej siv qhov muag pom, uas tshwm sim yuav luag tas li. Yog tias pom muaj tus kab mob raws sijhawm, ces koj tuaj yeem tshem tau qhov muag ntawm lub qhov muag los ntawm qhov muag, tsis yog siv rau txoj kev phais mob. Koj yuav tsum paub tias muaj ntshav qab zib, tsis yog tag nrho cov tshuaj siv tau, vim tias muaj ntau tus naj npawb ntawm cov kabmob thiab cov teebmeem.

• Nta ntawm cov kab mob qhov muag hauv ntshav qab zib
• Zam kev tsis pom kev hauv cov ntshav qab zib (yeeb yaj kiab)
• Yuav thov cov tee qhov muag rau hom 1 thiab ntshav qab zib hom 2: cov lus qhia pab tau
• Cov vitamins rau lub qhov muag mob ntshav qab zib
• Qhov muag npaj rau kev kho cov cataracts hauv ntshav qab zib
• Qhov muag nchuav rau kev kho kab mob glaucoma hauv ntshav qab zib
• Ophthalmic cov neeg sawv cev rau kev kho mob ntawm retinopathy mob ntshav qab zib

Nta ntawm cov kab mob qhov muag hauv ntshav qab zib

Kev puas tsuaj rau cov kab mob hauv lub cev tag nrho yog cov yam ntxwv ntawm tus kab mob ntshav qab zib, vim qhov tshwm sim ntawm cov hlab ntsha, cov hlwb thiab cov nqaij ntawm cov plab hnyuv siab raum raug mob.Nrog ntshav qab zib, cov kab mob qhov muag hauv qab no feem ntau tshwm sim:

1. Cataract, uas yog cim los ntawm clouding ntawm lub lo ntsiab muag. Hauv cov foos tshaj, tsuas yog yuav tsum muaj kev phais mob xwb.
2. Glaucoma yog, ib yam li tus kab mob dhau los, feem ntau tshwm sim hauv ntshav qab zib ntawm ib yam. Tawm tsam nws cov keeb kwm yav dhau los, cov kev phom sij txaus ntshai tshwm sim.
3. Keeb kwm yav dhau los retinopathy yog yus muaj kev puas tsuaj rau cov leeg hauv lub retina.
4. Txoj kev loj hlob ntawm tus neeg tshiab
5. Nrog maculopathy, macula yog puas lawm.

Cov kab mob ntawm cov cuab yeej siv kho qhov muag tiv thaiv ntshav qab zib mellitus muaj cov chav kawm sai. Yog li, nws yog ib qho tseem ceeb uas koj yuav tsum hu rau tus kws kho qhov muag kom tau txais kev pab tsim nyog ntawm thawj ntu. Cov tsos mob thawj zaug suav nrog qhov txo qis ntawm qhov pom, pom lub cev qhuav lossis lossis, hloov dua siab tshiab, cov av noo ntau ntxiv hauv cov qog ua kua thiab tsis xis nyob.

Yuav thov cov tee qhov muag rau hom 1 thiab ntshav qab zib hom 2: cov lus qhia pab tau

Txoj cai tseem ceeb thiab tsis tseem ceeb rau kev siv tshuaj daws qhov muag rau cov ntshav qab zib hom 1 thiab ntshav qab zib hom 2 yog kev teem caij thiab kev tshem tawm ntawm tus kws tshaj lij rau cov hauv paus ntawm kev ntsuas ntsuas.

Cov yam ntxwv tseem ceeb ntawm kev siv qhov muag npog rau cov ntshav qab zib:

1. Ua raws li cov kws kho mob qhia nruj.
2. Lub sijhawm kho yog txawv ntawm 2 lub lis piam mus rau 3, nyob ntawm tus kab mob pathology thiab chav kawm ntawm tus kab mob.
3. Nrog rau kev mob ntsej muag txhawm rau, qhov muag poob qis yog ib txwm sau rau kev kho mob ntev.
4. Qhov muag dauv tuaj yeem thiab yuav tsum tau nqus dej rau kev tiv thaiv.
5. Cov txheej txheem yog qhov tseem ceeb los nqa tawm tsuas yog ua tib zoo ntxuav tes.
6. Koj siv tsis tau ib tee ib zaug rau ob tug neeg. Lawv yuav tsum tshwj rau cov neeg siv xwb.
7. Them nyiaj tshwj xeeb rau lub txee lub neej, hnub tim ntawm kev tsim khoom, contraindications thiab kev phiv tshuaj nyob rau hauv cov lus qhia.
8. Yog tias koj tib lub sijhawm xau 2 lossis ntau dua kev siv tshuaj, nco ntsoov tuav lub sijhawm tsawg kawg li 15 feeb ntawm kev kho mob.
9. Tom qab qhov muag pom tseeb, yaug kom zoo thiab tsau cov roj av.
10. Yog tias thaum lub sijhawm instillation koj xav tias saj ntawm qhov kev daws - tsis txhob ceeb, qhov no yog ib qho kev coj ua, vim tias cov tshuaj ntws nkag tau yooj yim nkag mus rau hauv lub qhov ntswg qhov quav mus rau hauv lub qhov ncauj kab noj hniav thiab lub suab.

Yuav ua li cas drip kom raug:

• qhib lub hau, yog tias tsim nyog, coj cov raj dej huv,
• nyob rau qhov chaw xis - zaum los yog pw,
• qaij koj lub taub hau rov qab thiab sim maj mam muab rub daim npog sab hauv qab, ntsia qhov muag yuav tsum ncaj qha mus rau saum toj,
• txia nrog cov naj npawb uas yuav tsum tau ntawm cov tee rau hauv daim npog qis ze ze rau hauv lub ces kaum sab hauv ntawm lub qhov muag,
• tsis txhob cia lub pipette kov lub mucous daim nyias nyias thiab plaub muag,
• xa rov qab daim tawv muag rau nws qhov chaw nyob qub thiab npog koj lub qhov muag,
• txhawm rau txhim kho cov khoom faib ntawm cov tshuaj, maj mam zaws lub hnab ntim khoom plig,
• tshem cov tshuaj ntxiv nrog cov paj rwb so huv rau,
• ua kom koj lub qhov muag mus li ntawm ob peb feeb.

Cov vitamins rau lub qhov muag mob ntshav qab zib

Ua ntej tshaj plaws, muaj ntshav qab zib, kev teem caij noj tshuaj vitamin ua ntej rau lub qhov muag pom yog tsim nyog. Lawv yuav tsum muaj cov vitamins B1, B6, B2, E, A, C, tshuaj tua kab mob, tshuaj ntxhia thiab lwm yam tshuaj muaj txiaj ntsig. Ntawm qhov zoo tshaj plaws qhov muag npaj nrog cov vitamins yog cov hauv qab no:

Doppelherz Cov Khoom Siv (tshwj xeeb tshaj yog rau cov neeg mob ntshav qab zib) yog tus cwj pwm los ntawm kev hloov pauv ntawm cov tshuaj tsis haum thiab kev ua kom sai ntawm cov txheej txheem hauv cov khoom hauv qhov muag pom. Nws yog qhov tshwj xeeb tshaj yog siv lawv rau lub sijhawm ntev, raws li qhov xwm txheej dav dav ntawm cov ntshav qab zib nce siab.

Ophthalmo-DiabetoVit yog cov tshuaj zoo ua tau zoo ntawm cov tshuaj dhau los.

Lub Kuab Tshuaj Ntshav Qab Zib yog tsim los ntawm kev rho tawm ntawm cov nroj tsuag tshuaj. Tiv thaiv kev loj hlob ntawm cov teeb meem thiab qhov muag kab mob feem ntau.

"Alphabet Opticum" kuj tseem tsim nyob rau hauv cov khoom sib txuas ntawm cov khoom ntoo ib txwm muaj.

Qhov muag npaj rau kev kho cov cataracts hauv ntshav qab zib

Hauv qhov tso tawm, lub teeb ntawm qhov muag yog lub luag haujlwm rau clouding, uas yog lub luag haujlwm rau cov duab kho qhov muag. Cov kab mob qhov muag pib sai sai, tab sis nyob rau theem pib nws tuaj yeem kho tau los ntawm txoj kev kho qhov muag tshwj xeeb.Qhov nrov tshaj plaws thiab feem ntau kws kho mob txhais tau tias nyob rau hauv daim ntawv ntawm lub qhov muag rau ntshav qab zib mellitus ntawm ib yam:

1. "Taufon" lossis "Taurine" muaj cov kev tsim dua tshiab thiab rov them dua. Cov qog ua kua rau rov qab tau rov qab zoo li qub, cov kab mob dystrophic raug tshem tawm, cov metabolism sai dua thiab ua rau cov hlab ntsws ua kom yooj yim dua. Yuav luag tsis muaj kev phiv, tab sis kev fab tshuaj tsis haum tuaj yeem tshwm sim. Contraindication - muaj hnub nyoog txog 18 xyoo, ua xua rau cov Cheebtsam. Nws raug tso cai los nqus 2-4 zaug ib hnub rau 2 tee qhov siab tshaj plaws. Lub sijhawm tiv thaiv yog 90 hnub. Ib so yog lub hlis.
2. "Catalin" normalizes cov txheej txheem metabolic ncaj qha nyob rau hauv lub lens ntawm lub qhov muag, tiv thaiv kev txhim kho ntawm cataracts thiab hloov pauv ntawm qab zib rau hauv sorbitol, tawm tsam uas lub lens raug rhuav tshem. Thaum siv, ua qhov hnov ​​luv luv thiab khaus khaus, ntau dua cov kua muag, liab thiab ua xua tuaj yeem tshwm sim. Koj tuaj yeem nqeg dej txog 5 zaug hauv ib hnub, 2 tee. Lub chav kawm ntawm txoj kev kho yog raug txiav txim rau ib tus neeg ib qib.
3. Quinax muaj cov khoom xyaw tseem ceeb - azapentacene, ua tsaug uas cov txheej txheem metabolic yog qhib kom ua haujlwm, lub siab intraocular yog li qub thiab lub lens tawm tsis kam nrog oxidation nce. Ua tau zoo tshem tawm clouding ntawm lub lens, tsis muaj kev phiv tshuaj. Thov kev pab ntawm 3 mus rau 5 zaug hauv ib hnub, 2 tee. Lub sijhawm yog txiav txim los ntawm tus kws tshaj lij.

Nrog rau cov ntshav qab zib thiab tus mob cataracts, nws yog nruj me ntsis txwv tsis pub ua kev phais mob, yog li kev siv tshuaj kho yog suav tias yog tib txoj kev kho mob.

Qhov muag nchuav rau kev kho kab mob glaucoma hauv ntshav qab zib

Nrog rau kev ua pa txhawm rau lub ntsej muag, lub siab ceev ceev nce siab tuaj, ua rau tiav lossis ib nrab dig muag. Cov feem ntau siv qhov muag dauv yog:

1. “Yopidin”, “Alfagan R”, “Luxfen”, “Brimonidin”, “Combigan”. Cov tee no txo ​​qhov kev tsim tawm ntawm cov kua dej ua haujlwm, txhim kho kev tawm, uas ua rau txo lub zog intraocular. Tshuaj yog alpha adrenergic receptor agonists.
2. “Timolol”, “Trusopt”, “Betoptic”, “Levobunolol”, “Xonef”, “Betaxolol”. "Metipranolol" muaj cov beta blockers.
3. Dorzolamide, Brinzolamide ua raws li carbonic anhydrase inhibitors.
4. "Pilocar", "Physostigmine." Tshuaj yuav rau myotics.
5. "Lumigan", "Travoprost", "Latanoprost" - prostaglandins.

Ophthalmic cov neeg sawv cev rau kev kho mob ntawm retinopathy mob ntshav qab zib

Nrog rau retinopathy, qhov kev hloov ncig ntawm lub qhov muag cuam tshuam, vim qhov tshwm sim ntawm qhov twg pathological kev cuam tshuam hauv retina ntawm qhov muag pom cov cuab yeej tau sau tseg. Cov tshuaj pleev qhov muag hauv qab no yog siv:

1. Ib pawg tshuaj uas tsim los kho mob cataracts (teev saum toj no).
2. "Emoksipin" pab nrawm cov ntshav ncig thiab cov metabolism, neutralizes lub hemorrhage resulting. Kev phiv tshuaj suav nrog kev hlawv thiab khaus. Thov ob zaug ib hnub, 2 tee rau ib hnub.
3. "Holo-hauv siab" neutralizes dryness. Nws siv nws peb zaug ib hnub.
4. Riboflavin feem ntau kho mob ntshav qab zib hom 2. Muaj cov vitamins B, normalizes hemoglobin synthesis. Nws nrawm nrawm mus rau qhov metabolism. Txhim kho txoj haujlwm ntawm cov khoom siv kom pom. Txw los yog tso cai tsis ntau tshaj 1 poob 2 zaug hauv ib hnub. Cov kev mob tshwm sim - luv luv txo nyob rau hauv pom thiab pom kev ua xua.
5. Lacamox moisturizes thiab muag muag, muaj kev tiv thaiv zoo rau lub pob txha caj qaum thiab mob caj dab. Txhawb nqa resorption ntawm cov hemorrhages nyob rau hauv lub qhov muag pom lub tshuab, txo qhov degree ntawm o, rov kho lub qog retinal. Cov Tshuaj Tiv Thaiv - kev xeeb tub, kev fab tshuaj rau cov Cheebtsam. Tom qab siv, nws ua rau khaus khaus thiab hlawv. Koj tuaj yeem siv peb zaug ib hnub rau 2 tee.

Nws yog ib qho tseem ceeb uas yuav tau them sai sai rau cov tsos mob uas qhia txog kev txhim kho ntawm cov kab mob qhov muag kom raws sijhawm. Nco ntsoov, mus rau hauv lub tsev kho mob thaum pib thiab ua tib zoo saib xyuas txhua tus kws kho mob sau ntawv yuav ua rau koj zam kev rau qhov tsis zoo - los ntawm kev txo qhov muag pom kom tiav qhov muag tsis pom!

Analogues ntawm cov tshuaj

Thaum qee leej neeg tsis quav ntsej rau cov neeg sib cais "Emoksipin" lossis rau lwm qhov laj thawj uas ua rau nws tsis tuaj yeem siv cov tshuaj ntws, cov kws kho mob tau muab tshuaj rau cov tshuaj zoo ib yam li cov tshuaj yeeb dej caw. Cov kws tshuaj hauv qab no tuaj yeem hloov "Emoksipin":

Rov qab rau cov lus txheej txheem

Cov Neeg Ua thiab Teeb Meem Qhov Tseeb

Tus mob retinopathy yog ib feem ntau ntawm cov neeg mob ntshav qab zib. Tus kab mob no yog qhov tseem ceeb ua rau muaj kev puas tsuaj rau cov hlab ntsha retinal. Yog tias cov ntshav qab zib muaj txog li 2 xyoo, kab mob pathology raug kuaj pom hauv 15% ntawm cov neeg mob, 15 xyoo - 50%, 25 xyoo lossis ntau dua - qhov kev tshwm sim nce mus txog 100%.

Tus nqi ntawm kev muaj mob ntawm cov ntshav qab zib retinopathy nyob ntawm qhov pom tseeb ntawm kev kho mob etiological, nrog rau kev mob cuam tshuam. Lub pathology ntawm cov hlab ntsha retinal muaj kev nrawm dua yog tias tus neeg mob ib txhij tiv thaiv los ntawm kev cuam tshuam xws li:

• dyslipidemia,
• rog dhau
• metabolic mob
• mob raum tsis ua hauj lwm
• ntshav siab.

Qhov teeb meem cuam tshuam hauv kev txhim kho mob ntshav qab zib retinopathy tuaj yeem yog cev xeeb tub, tus cwj pwm tsis zoo (haus luam yeeb), nkauj tiav nraug, muaj mob muaj keeb thawj.

Theem Kab Mob Ntshav Qab Zib Retinopathy

Nyob ntawm qhov kev hloov pauv pathological, 3 theem ntawm tus kabmob muaj qhov txawv:

Kuv - non-proliferative retinopathy. Nws yog nrog los ntawm o ntawm cov retina hauv thaj av ntawm macula, microaneurysms, foci ntawm exudation, hemorrhage raws cov leeg, hauv qhov chaw ntawm lub pob txha yog pom hauv lub retina.

II - preproliferative mob ntshav qab zib retinopathy. Ntau yam retinal hemorrhages, paj rwb thiab khoom exudates yog cov yam ntxwv. Pom meej ua kom pom kev hloov ntawm cov qauv ntawm lub qhov muag leeg.

III - kev loj hlob rov qab zoo dua. Neovascularization ntawm optic hlab ntsha disc tshwm sim. Ntawm thaj chaw ntawm preretinal hemorrhage, fibrous cov ntaub so ntswg. Feem ntau txhim kho retinal detachment, Secondary glaucoma.

Kev phom sij ntawm tus mob ntshav qab zib retinopathy yog tias ntev ntev nws tsis nrog kev tshwm sim pathological. Nyob rau lub sijhawm tsis hloov pauv vim muaj mob ntawm tus neeg mob macula, tsuas yog ua rau cov khoom tsis pom kev, teeb meem hauv kev ua haujlwm ntawm qhov chaw nyob ze rau lub qhov muag, piv txwv li, thaum nyeem, yuav cuam tshuam.

Hauv cov qib loj zuj zus ntxiv, cov quav ntshav tshwm tuaj, lawv ua rau daim ntaub thaiv, daim tawv ntab ntab, uas ploj zuj zus. Yog tias muaj teeb meem ntshav tseem ceeb, muaj qhov txo qhov muag pom kiag thaum ua tiav qhov muag tsis pom kev.

Kev kuaj mob

Txij li thaum tus kab mob ntshav qab zib ua tsis yog kev kho mob hauv cov theem pib, tab sis yuav tsum tsim muaj cov ntshav qab zib mellitus, cov neeg mob uas kuaj pom no yuav tsum tau mus kuaj mob nrog kws kho qhov muag tshwj xeeb. Rau lub hom phiaj ntawm kev paub ua ntej, kev tshawb fawb zoo li no tau sau tseg:

• Qhuas
• biomicroscopy
• ophthalmoscopy nyob rau hauv mydriasis,
• perimetry
• kho qhov muag tau tomography,
• tonometry.

Kev soj ntsuam ntxiv nyob ntawm saib cov nyiaj uas tau txais. Kev kuaj pom lub qhov muag ntawm lub qhov muag yog tsim thaum pom ntawm lub cev ntawm lub cev thiab lens tau kuaj pom. Txhawm rau txiav txim siab ua haujlwm ntawm lub teeb tsa optic thiab retina, nws tau raug sau tseg:

• kev txiav txim siab ntawm CFSM,
• electroretinography,
• duab hluav taws xob.

Gonioscopy yog siv rau cov kab mob neovascular glaucoma. Txhawm rau pom cov hlab ntsha ntawm kev pab retina:

• fluorescence angiography,
• laser scanning tomography.

Cov neeg uas ntxim yuav tsim muaj cov ntshav qab zib retinopathy yuav tsum muaj kev soj ntsuam ib ntus los txiav txim siab lipid profile. Kuj, kev soj ntsuam txhua hnub, ECG, echocardiography, ultrasound ntawm cov hlab ntsha muab khoom rau lub raum tuaj yeem kho tau.

Kev Kho Mob Retinopathy Mob Ntshav Qab Zib

Cov neeg mob tau sau tseg kev kho mob nyuaj, uas yog nyob ntawm theem ntawm tus kab mob thiab qhov muaj cov kab mob sib kis. Nco ntsoov nqa tawm txoj kev kho ntawm cov kab mob tseem ceeb - ntshav qab zib mellitus, xaiv cov tshuaj ntawm cov tshuaj insulin yog xaiv. Cov tsos mob kho tau kuj yog kws kho:

• cov neeg ua haujlwm antiplatelet
• angioprotectors
• antihypertensive tshuaj.

Yog hais tias tus mob ntshav qab zib retinopathy nrog macular edema, intravitreal tswj hwm ntawm cov tshuaj steroid yog nqa tawm. Tam sim no, ntau thiab ntau laser kev cuam tshuam tau ua. Txoj kev ua no tso cai rau koj txhawm rau tshem tawm neovascularization, zam kev ua kom lub ntsej muag, thiab ua kom tiav cov ntshav ntawm cov hlab ntsha.

Laser coagulation tau nqa tawm hauv ntau hom:

• teeb meem - yog siv rau cov tsis muaj hom ntawm cov kabmob thiab macular edema,
• focal - qhia rau siv nyob rau kis yog kuaj pom pob qij txha, mob pob txha nqaj ntshav, exudates.

Yog tias qhov mob ntshav qab zib retinopathy nrog cov teeb meem nyob rau hauv daim ntawv ntawm retinal detachment, hemophthalmus thiab lwm yam mob, vitrectomy yog qhia - tshem tawm ntawm lub cev vitreous, hemorrhage, dissection ntawm cords ntawm cov nqaij mos txuas.

LLC Lag Luam "FERMENT"

1 ml ntawm kev daws

Cov khoom kom nquag: Methylethylpyridinol hydrochloride (emoxypine) - 10 mg,

Cov zam: anhydrous sodium sulfite - 3.0 mg, sodium benzoate - 2.0 mg, potassium dihydrogen phosphate - 6.2 mg, sodium hydrogen phosphate dodecahydrate - 7.5 mg, methyl cellulose 5.0 mg, dej rau kev txhaj tshuaj - txog 1 ml Cov.

Kev taw qhia rau kev siv:

• kev kho thiab kev tiv thaiv ntawm o thiab hlawv ntawm lub pob zeb,
• kev kho mob hemorrhages nyob rau hauv chav ua ntej ntawm lub qhov muag,
• kev kho mob thiab kev tiv thaiv kev mob hemorrhage hauv sclera hauv cov neeg laus
• thrombosis ntawm hlab ntsha nruab nrab ntawm Retina thiab nws cov ceg,
• kho cov teeb meem ntawm myopia,
• kev tiv thaiv ntawm lub pob taws thaum hnav tsom iav,
• uas yog kuaj ntshav qab zib.

Kev twv ua ntej thiab Kev Tiv Thaiv

Kev ntsuas rau tus mob ntshav qab zib retinopathy nyob ntawm theem ntawm cov kab mob uas tau kuaj pom, thiab kev muaj txiaj ntsig ntawm kev kho tau. Cov txiaj ntsig tau zoo yog qhia los ntawm prophylactic laser coagulation nyob rau theem preproliferative. Kev kho ntshav qab zib kom zoo thiab kev soj ntsuam ntshav qabzib tas li kuj tseem tuaj yeem pab ncua qhov pib ntawm qhov muag tsis pom.

Kev tiv thaiv ntawm tus kab mob ntshav qab zib retinopathy muaj nyob rau hauv kev tshuaj xyuas kab mob ntshav qab zib mellitus tas li ntawm kev muaj mob caj dab, txaus kho tus kab mob concomitant. Qhov tsis txaus ntseeg tshaj plaws rau kev sib xyaw ntawm pathology nrog kub siab thiab atherosclerosis.

Emoxipin Txhaj Tshuaj

Tsoomfwv Tsoomfwv Tebchaws Lub Tsev Haujlwm Tsis Txaus Siab "Moscow Endocrine Cog"

1 ml ntawm kev daws

Cov khoom kom nquag: Methylethylpyridinol hydrochloride (Emoxipine) - 10 mg,

Cov muaj mob: hydrochloric acid 0, 1 M, dej rau txhaj

Kev taw qhia rau kev siv:

• Kev koom ua ke thiab kev sib txuam ntawm ntau lub hauv paus,
• Angioretinopathy (suav nrog kev mob raum retinopathy),
• Nruab nrab thiab ntu txhauv chorioretinal dystrophy, suav nrog cov myopia nyuaj,
• Mob ntsws nruab nrab ntawm cov leeg ntshav nraub qaum thiab nws cov ceg ntoo,
• Qhov muag phais, mob tom qab kev phais kab mob rau lub ntsej muag nrog choroid detachment,
• Dystrophic kab mob ntawm lub pob zeb,
• Raug mob, o thiab kub ntawm lub qhov muag,
• Kev tiv thaiv ntawm lub qhov muag (thaum hnav tsom iav) thiab retina ntawm lub qhov muag los ntawm kev sib chwv sib zog (lub teeb ci thiab lub hnub ci, nrog laser coagulation).

Cov ntsiab lus ntawm cov lus pom zoo ntawm cov neeg sib tw ntawm kev kho mob science Volkova, Natalya Anatolevna

Mob ntshav qab zib mellitus yog qhov muaj feem thib 1 ntawm cov teeb meem ntsib kev kho mob thiab kev kho mob hauv yuav luag txhua lub teb chaws hauv ntiaj teb. Nyob rau hauv xyoo tas los no, muaj qhov nce ntawm cov neeg mob ntshav qab zib mellitus, nce txhua xyoo los ntawm 6-10%, thiab yog li ntawd, tag nrho cov neeg mob hauv Lavxias teb chaws nce mus txog 2-4% ntawm tag nrho cov pejxeem (Balabolkin MI, 2000, Dedov I.I. ., 2002). Nrog rau cov kab mob plawv thiab ntshav oncological, ntshav qab zib mellitus pib koom nrog pathology feem ntau ua rau kev xiam oob qhab thiab kev tuag ntawm cov neeg mob (Shestakova MV, 2000, Saltykov BB, 2001).

Txawm hais tias muaj kev nyuaj ntawm cov pathogenesis ntawm kev mob lig ntawm ntshav qab zib mellitus, qhov chaw tseem ceeb hauv lawv cov kev pib thiab kev vam meej belongs rau cov mob hyperglycemia, thiab yog li ntawd, lub hom phiaj tseem ceeb ntawm kev kho ntshav qab zib yog kom ua tiav lub sijhawm ntev thiab ruaj khov rau cov metabolism metabolism. Txawm li cas los xij, txoj kev kho nyuaj ntawm cov kab mob no ua tsis tiav yam tsis muaj kev siv tshuaj uas cuam tshuam rau lwm cov kab mob pathogenetic hauv kev txhim kho thiab kev loj hlob ntawm cov kab mob ntshav qab zib, qhov tseem ceeb tshaj plaws uas yog dyslipidemia. Sim los cuam tshuam txhua yam ntawm ntau qhov txuas hauv pathogenesis ntawm ntshav qab zib mellitus, tus kws kho mob, hmoov tsis, yog inexorably kos rau hauv polypharmacy, nyob rau hauv kev twb kev txuas nrog uas tus naj npawb ntawm tsis tsuas yog phiv, tab sis kuj thiav nce (Nerup J., 1994, Marse J. B. li al. , Xyoo 2001).

Yog li ntawd, kev xaiv yog muab rau cov tshuaj nrog cov ua ke, cov kev xaiv uas tsis zoo: cov no yog sulfonylurea derivatives (Aschcroft F. M. et al., 2001), biguanides (Jansen M. et al., 1991) thiab thiazolidinedione derivatives (Sato Y. et al. ., 1999).

Ntau yam ntawm cov kev mob tshwm sim thiab meej contraindications txwv kev siv ntau ntawm cov tshuaj no nyob rau hauv kev soj ntsuam xyaum. Kev siv cov sulfonylurea derivatives yog txwv los ntawm kev txhim kho ntawm kev tiv thaiv kab mob thib ob rau lawv hauv 5-10% ntawm cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus (Aleksandrov A.A., 2001). Qhov kev txwv ntawm kev siv cov biguanides yog txiav txim siab los ntawm kev muaj peev xwm tsim cov kab mob lactic acidosis (Witztum J.L., 1992), thiab thiazolidinedione derivatives nrog qhia tawm hepatotoxicity (Forman L.M., li al., 2000).

Txhua qhov tseeb no ua rau nws pom tseeb tias yuav tsum tau tsim cov tshuaj tshiab uas muaj txiaj ntsig zoo, muaj kev tiv thaiv kev tiv thaiv kab mob, vim tias tsuas yog nthuav cov ntau ntawm cov tshuaj tiv thaiv kab mob hauv qhov ncauj yuav ua kom ntau tshaj ntawm cov nyiaj mob ntshav qab zib coj mus rau hauv tus account tus yam ntxwv ntawm txhua tus neeg mob, txhim kho lub neej zoo ntawm cov neeg mob, txo kev ua tsis taus, tswj kev ua haujlwm ntawm cov neeg mob ntshav qab zib, uas muaj ntau kev hais lus tseem ceeb ntawm tib neeg rau lub neej.

Lub neej yav tom ntej belongs rau cov tshuaj uas tuaj yeem tshwj xeeb rau cov kab mob tseem ceeb ntawm kev sib kis kab mob thiab muab kev muaj peev xwm tiv thaiv thiab kho ntawm cov teeb meem vascular cov ntshav qab zib. Muab lub luag haujlwm tseem ceeb ntawm kev ua haujlwm ntawm dawb radical oxidation kev ua hauv pathogenesis ntawm ntshav qab zib mellitus thiab nws cov teeb meem vascular (Balabolkin M.I. et al., 1999, Korchin V.I., 2000, Bondar I.A. et al., 2001, Fadeeva N.I. et al., 2001), tshuaj tiv thaiv antioxidant ntawm hom kev ua yuav yog chav qhia tshuaj lom neeg muaj txiaj ntsig zoo rau cov kev tshawb fawb no. Hauv kev mob ntshav qab zib, kev paub tau nce nrog kev siv ntau ntawm cov tshuaj nrog cov kev ua antioxidant, suav nrog nicotinamide (Gorelysheva V.A. et al., 1996, Bondar I.A. et al., 2001, Kolb N. et al., 1999, Pozzilli et al., 1999), a-tocopherol (Ceriello A. li al., 1991,

Pozzilli P. et al., 1997, Frei B., 1999, Bursell S.E. et al., 1999, Emmert D. M. li al., 1999), kua qaub lipoic (Balabolkin M.I. li al., 2000). Xyoo tsis ntev los no, kev txaus siab ntawm cov kws tshawb nrhiav thiab cov kws kho mob hauv cov pab pawg dej-soluble antioxidants, uas suav nrog cov derivatives ntawm 3-hydroxypyridine, uas tuaj yeem ua rau ntau qhov txuas ntawm pathogenesis ntawm ntshav qab zib mellitus ib zaug, tau nce. Raws li cov ntaub ntawv (Grechko A.T., li al., 1998, Smirnov L.D., 1998, Nelaeva A.A., 1999, Lukyanova L.D., 1999, 2000, 2002,, T. Devyatkina et al., 2000, V. Yasnetsov li al., 1999) thiab cov txiaj ntsig ntawm kev tshawb fawb yav dhau los (V. Inchina li al., 1996, 2000, A. V. Zorkina, 1997, 1999, L.N. Sernov ., 1996, 1998, Spasov A.A. et al., 1997, 1999, Nazipova D.A. et al., 1998, Vintin N.A., 1999, Mikhin V.P. li al., 1998, 2002 , Mironov N.V. li al., 2002, Katikova O.V. li al., 2002 thiab lwm tus), cov khoom sib txuas ntawm cov tshuaj lom neeg no muaj pov thawj hypoglycemic, hypolipidemic, antioxidant, antihypoxic, anticoagulant Nau-a, antithrombogenic, antiplatelet, immunomodulatory, membrane-tiv thaiv nyhuv. Yog li, kev tshawb nrhiav cov tshuaj muaj peev xwm tiv thaiv kab mob nrog rau cov txiaj ntsig ntawm kev sib txuas ntawm 3-hydroxypyridine yog qhov tsim nyog thiab tsim nyog.

Lub hom phiaj tseem ceeb ntawm txoj kev tshawb no yog kawm txog cov txiaj ntsig mexidol thiab emoxipin ntawm qee cov teeb meem metabolic raws cov kev sib xyaw ua ke ntawm kev sim hyperglycemia thiab exogenous hypercholesterolemia hauv kev sim tsiaj, zoo li hauv cov ntshav ntawm cov neeg mob uas muaj hom 2 ntshav qab zib mellitus.

Raws li cov hom phiaj hauv kev ua tau zoo ntawm cov haujlwm no, cov haujlwm hauv qab no tau daws:

1. Txhawm rau kawm cov nyhuv ntawm mexidol, emoxipin, dimephosphone thiab a-tocopherol ntawm glycemia, qee qhov ntsuas ntawm lipid thiab protein metabolism hauv kev sim ntshav qab zib mellitus hauv kev sib xyaw nrog exogenous hypercholesterolemia.

2. Txhawm rau kawm txog cov nyhuv ntawm cov tshuaj ntawm lipid peroxidation cov txheej txheem thiab lub xeev ntawm cov kab mob antioxidant hauv cov ntshav ntshav thiab cov nqaij ntawm kev sim cov tsiaj nyob hauv cov xwm txheej ntawm simulated pathology.

3. Yuav kawm txog kev hloov pauv hauv kev siv tshuaj lom neeg ntawm myocardium nyob rau keeb kwm yav dhau los ntawm kev siv tshuaj tiv thaiv tshuaj tua kab mob hauv cov tshuaj tiv thaiv kab mob sib xyaw ua ke ntawm kev sim ntshav qab zib mellitus thiab hypercholesterolemia.

4. Txhawm rau kawm txog cov txiaj ntsig mexidol, emoxipin thiab dimephosphon ntawm qib glycemia, qib ntawm glycation ntawm hemoglobin, lub xeev ntawm lipid peroxidation system hauv cov ntshav ntshav thiab cov ntshav liab ntawm cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus hauv vitro.

Kev tsim qauv tshiab ntawm kev ua haujlwm

Cov txiaj ntsig ntawm mexidol, emoxipin, dimephosphone thiab a-tocopherol ntawm lub xeev ntawm carbohydrate, lipid, protein metabolism, lipid peroxidation thiab cov kev ua haujlwm ntawm cov kab mob antioxidant hauv cov ntshav ntshav thiab cov nqaij ntawm kev sim tsiaj tau kawm nyob rau hauv kev sib xyaw ua ke ntawm kev sim ntshav qab zib mellitus thiab exogenous hypercholesterolemia, thiab nws tau qhia tias mexidol hypoglycemic thiab antioxidant cuam tshuam, qhia hauv kev sib piv nrog dimephosphone thiab a-tocopherol.

Thawj thawj zaug, nws tau qhia tias mexidol, emoxipine thiab dimephosphon, thaum ua ke nrog ntshav qab zib mellitus thiab hypercholesterolemia, kho qhov hluav taws xob tsis khov ntawm myocardium, pab kho qhov teeb meem bioelectric ntawm myocardium.

Nws tau pom thawj zaug tias muab cov ntshav rau cov neeg mob ntshav qab zib mexidol thiab emoxipin txo cov ntshav glycemia thiab inhibits hemoglobin glycation hauv vitro. Kev tsim cov ntshav nrog cov kev kawm txog tshuaj tiv thaiv kab mob antioxidant txwv lipid peroxidation (tshwm sim thiab cov hlau tsim), ua kom lub xeev muaj cov kab mob antioxidant hauv cov ntshav ntshav thiab erythrocytes ntawm cov neeg mob ntshav qab zib. Qhov siab tshaj plaws tau tshwm sim thaum Mexidol tau nkag mus rau hauv kev sib xyaw nrog sib xyaw.

Cov txiaj ntsig ntawm kev ua haujlwm

Cov txiaj ntsig ntawm txoj kev tshawb no nthuav kev nkag siab ntawm lub chaw muag tshuaj ntawm mexidol, emoxipin, dimephosphone thiab a - tocopherol. Ntawm cov nqi tseem ceeb yog cov ntaub ntawv ntawm lub peev xwm ntawm kev kawm txog tshuaj tiv thaiv kab mob antioxidant los txhim kho kev cuam tshuam ntawm cov carbohydrate, lipid, protein metabolism, hluav taws xob myocardial tsis khov nyob rau hauv kev sib xyaw ua ke ntawm kev sim ntshav qab zib mellitus thiab hypercholesterolemia.

Cov ntaub ntawv tau txais tuaj yeem siv rau kev kawm ntxiv txog kev cuam tshuam ntawm cov tshuaj hauv lub cev nrog rau kev sib xyaw ntawm cov kev pheej hmoo no.

Cov txiaj ntsig ntawm kev tshawb fawb tawm suab tau ntxiv rau hauv kev tshawb nrhiav kev ua haujlwm ntawm Lub Tsev Haujlwm Saib Xyuas Tshuaj ntawm Mordovia State University.

Cov Ntsiab Lus Tseem Ceeb rau Kev Tiv Thaiv

1. Cov kev saib xyuas ntawm 3-hydroxypyridine ua tau zoo tshaj plaws nyob rau hauv kev sib piv nrog dimephosphone thiab a-tocopherol kho cov teeb meem tsis sib haum ntawm carbohydrate, protein thiab lipid metabolism nyob rau hauv kev sib txuas ua ke ntawm kev sim ntshav qab zib thiab exogenous hypercholesterolemia.

2. Txhua tus kawm txog tshuaj tiv thaiv antioxidant tiv thaiv kev txhim kho ntawm myocardial hluav taws xob tsis txaus, txo kev tawg ntawm QT luv.

4. Mexidol hauv cov koob tshuaj kawm thiab emoxipin muaj cov txiaj ntsig los tiv thaiv kev tshaj tawm, tiv thaiv kev ua haujlwm ntawm lipid peroxidation cov txheej txheem thiab kev nyuaj siab ntawm cov kab mob antioxidant hauv cov ntshav ntshav thiab cov nqaij ntawm kev sim tsiaj nrog kev sib xyaw ua ke ntawm ntshav qab zib mellitus thiab exogenous hypercholesterolemia.

5.Mexidol ntawm koob tshuaj 0.025 mg / ml, muaj qhov siab tshaj plaws hypoglycemic, antioxidant nyhuv, feem ntau muaj kev tiv thaiv zoo rau hemoglobin glycation cov txheej txheem, lipoperoxidation (tshwm sim thiab Fe-induced) cov txheej txheem hauv cov ntshav ntshav thiab cov ntshav liab ntawm cov neeg mob thaum lub cev nrog ntshav ntawm cov neeg mob ntshav qab zib mellitus hom hauv vitro.

Cov kev tshawb nrhiav pom thiab cov kev cai tseem ceeb tau nthuav tawm hauv kev tshaj tawm tau tshaj tawm ntawm lub rooj sib tham ntawm cov tub ntxhais hluas tshiab ntawm Mordovia State University. N.P. Ogareva (Saransk, 2002), X Lavxias National Congress "Tus txiv neej thiab Tshuaj" (Moscow, 2003), 2nd Congress ntawm Pharmacologists ntawm Lavxias Federation (Moscow, 2003), XXXI Ogarev Nyeem Ntawv (rooj sab laj kev tshawb fawb ntawm N.P. Mordovian State University Ogareva, Saransk, 2003).

Kev nthuav tawm Ntawm cov ncauj lus ntawm kev hais tawm tshaj tawm kev ua haujlwm.

Kev ntsuas thiab kev teeb tsa ntawm kev ua haujlwm

Cov lus tshaj tawm no muaj qhov kev taw qhia, kev tshuaj xyuas ntawm cov ntawv nyeem, peb tshooj, uas tau teeb tsa cov txiaj ntsig ntawm peb tus kheej kev tshawb fawb, kev sib tham ntawm cov txiaj ntsig, cov lus xaus thiab cov npe teev tseg. Cov haujlwm tau teeb tsa ntawm nplooj ntawv sau, kos duab nrog cov duab kos thiab cov ntxhuav. Cov bibliographic sau muaj cov npe ntawm cov ua haujlwm, suav nrog cov kws sau hauv tsev thiab txawv teb chaws.

Tshooj Lus 1. Rov nyeem ntaub ntawv

1.1. Cov tswv yim niaj hnub hais txog lub pathogenesis ntawm ntshav qab zib.

Lub luag haujlwm ntawm lipid peroxidation hauv pathogenesis ntawm ntshav qab zib.

Pharmacotherapy ntawm cov ntshav qab zib mellitus yog txoj haujlwm kho mob nyuaj, hauv kev daws teeb meem uas nws yog ib qho tsim nyog yuav tsum coj mus rau hauv tus account cov yam ntxwv ntawm kev txhim kho ntawm cov txheej txheem pathological. Tam sim no, yam mob ntshav qab zib mellitus tau raug suav tias yog kev muaj mob caj ces, nyob rau hauv qhov tshwm sim thiab kev loj hlob ntawm qhov kev tiv thaiv kab mob autoimmune yog qhov tseem ceeb tshaj plaws (Balabolkin MI, 2000, Baker J. R., 1997). Hauv qhov no, kev puas tsuaj rau p - hlwb ntawm tus txiav yuav tshwm sim ob qho tib si los ntawm kev sib kis ncaj qha, thiab vim muaj microcirculatory cuam tshuam hauv qhov kev txiav txim siab (Bobyreva L.E., 1998). Lub tshuab autoimmune ntawm qhov tshwm sim ntawm hom ntshav qab zib muaj qhov caj ces cuam tshuam nrog caj ces ntawm HLA system (Conrad D., li al., 1997). Cytokines koom rau hauv kev siv ntawm kev tiv thaiv kev tiv thaiv kev tiv thaiv kabmob (Chung Y. N., 1999), uas cuam tshuam kev cuam tshuam kev cuam tshuam thiab ua rau muaj kev cuam tshuam ntawm cov lwg me me ntawm lub ntsiab histocompatibility ua rau (3 lub hlwb). Ib qho kev ua haujlwm ntawm lub cev tiv thaiv kab mob nrog nrog kev nce siab dawb radical tshua nrog kev tsim cov tshuaj lom neeg, kev puas tsuaj thiab apoptosis ntawm pancreatic P hlwb (Gorelysheva VA, 1999, Azizova OA, 2001, Ametov AS, 2001, Kaneto Hideaki li al., 1995, Dandona P., 1996). lub sijhawm, caj ces ntawm ntshav qab zib - hom tsis ua ntawm qhov kev xav txog niaj hnub no, ob txoj kev xaiv tau raug txiav txim siab: thawj - ob lub noob ywj siab koom nrog pathogenesis ntawm tus mob ntshav qab zib hom 2. Ib qho yog lub luag haujlwm rau qhov tsis txaus siab insulin, qhov thib ob - ua rau kev txhim kho ntawm insulin kuj. lossis cov ntaub so ntswg (Dedov II, et al., 2002).

Qhov tseem ceeb pathogenetic nyob rau hauv kev txhim kho ntawm cov ntshav qab zib hom 1 yog qhov kev txo qis ntawm cov kua dej los ua ke, uas cuam tshuam rau cov metabolism hauv lub ntsej muag, uas tau ua raws li ob qho kev qhia. Ua ntej, kev sib txuas ntawm diacylglycerol nce, uas cuam tshuam rau kev ua haujlwm ntawm Na / K-ATPase, thiab tseem ua rau kev ua haujlwm ntawm cov ntshav enzymes tsis ua haujlwm, uas txo cov qib ntawm fructose-2, -phosphate, txo glycolysis thiab txhim kho gluconeogenesis (Ishii N., 1998, Kim SJ et al. ., 1998). Qhov thib ob, polyol pauv txoj hauv kev yog ua kom nrog kev tsim ntawm sorbitol, uas tseem yuav txo qhov kev ua ntawm Na / K - ATPase. Kev hloov pauv tom qab ntawm sorbitol rau fructose, uas yog cov txheej txheem rau cov txheej txheem glycosylation, txhim kho parametolic (tsis-enzymatic) kev cuam tshuam, uas yog raws li kev tsim cov khoom lag luam glycosylation nyob rau theem ntawm enzymes, glycosaminoglycans ntawm cov qog ua ntshav thiab cov ntshav protein.

Cov txheej txheem ntawm lipid peroxidation muaj feem xyuam nrog kev hloov pauv parametolic, txij li muaj qhov sib cuam tshuam ncaj qha ntawm cov qib ntawm autooxidation cov khoom thiab qhov mob vascular cuam tshuam (Bobyreva L.E., 1996, Verbova N.I. et al., 1997, Chernov Yu.N. li al. Xyoo 1999, Hori O. et al., 1998, Brownlee M., 1999, Brownlee M. 2000).

Dawb radical lipid oxidation yog qhov tseem ceeb ntawm ntau cov txheej txheem tseem ceeb, xws li hloov hluav taws xob los ntawm flavin cov ntsiab lus, txuas ntxiv ntawm lipid muaj pes tsawg leeg ntawm biomembranes, phosphorylation oxidative phosphorylation nyob rau hauv mitochondria, mitogenesis, lub zog ua kom sib luag, thiab lwm yam (Lankin V.Z. li al., 2000, Halliwell) V., 2000). Cov khoom lag luam ntawm lipid peroxidation (lipid peroxidation) yog qhov ua ntej ntawm prostaglandins thiab lawv cov derivatives - thromboxanes thiab prostacyclin (Kagan V.E., li al., 1992). Cov tshuaj tiv thaiv peroxidation tsis tu ncua tshwm sim hauv cov xias ntawm tes ua rau muaj kev rov ua dua tshiab ntawm lawv cov lipid thiab kev saib xyuas ntawm cov haujlwm ua haujlwm ntawm txhua qhov lipid-dependen-enzymes, uas suav yuav luag txhua qhov system enzyme ntawm lub cev (Voskresensky ON, 1986, Dubinina E.E., 1995, Burlakova E.N. ., 1998, Lankin V.Z., et al., 2000, Morugova T.V., 2000, Velichkovsky B.T., 2001).

Raws li tus naj npawb ntawm cov sau phau ntawv, kev tsim cov pa oxygen dawb ntau dhau los cuam tshuam los ntawm cytokines ua si lub luag haujlwm tseem ceeb hauv pathogenesis ntawm ntshav qab zib mellitus. Cytokines xws li interleukin-1, kev mob qog necrosis thiab γ-interferon tuaj yeem cuam tshuam rau insulin secretion thiab muaj cov teebmeem cytotoxic rau p-hlwb ntawm tus txiav hauv vitro (Smirnova OM, Gorelysheva V.A. 1999).

Kev tshaj tawm ntawm oxygen oxygen radicals yog zais zais los ntawm cov macrophages thiab ua kom cov P hlwb puas (Kroncke K.D., li al., 1991, Burkard V., li al., 1992, Madndrup - Poulsen T., li al., 1993). Islet hlwb muaj cov kab mob tiv thaiv tsis muaj zog thiab yog qhov tshwj xeeb tshaj tawm rau cov dawb radicals, uas yog lub laj thawj tseem ceeb rau lawv cov lysis hauv cov ntshav qab zib mellitus (Kogan A.Kh., 1999, Asayama K., li al., 1996). Kev txhim kho ntawm lipid peroxidation cov txheej txheem tau lees paub cov kev sim ntawm cov qauv mob ntshav qab zib mellitus nrog alloxan thiab streptozotocin.

Cov nyhuv ntshav qab zib yog txiav txim siab los ntawm tropism ntawm alloxan rau P - hlwb thiab raug txo qis rau lawv qhov kev puas tsuaj (Karagezyan K.G., Hovsepyan L.M., Adonts K.G., 1990, Fridovich I., 1992). Lub tropism ntawm alloxan cuam tshuam nrog nws kev sib raug zoo rau qhov tshwj xeeb, txais tau qhov tseeb nkaus xwb rau P - hlwb, kev npaj ntawm SH membrane pawg nrog kev kawm siab ntawm ionization, ib puag ncig hauv thaj av ntawm cov receptors. Qhov zoo sib xws ntawm cov qauv molecular ntawm qabzib thiab alloxan, muaj cov nitrogen atoms thiab pawg carbonyl hauv nws cov qauv, ua kom muaj kev cuam tshuam ntawm alloxan nrog SH - pawg ntawm cov ntshav qabzib receptors thiab nws txoj kev ywj pheej mus rau hauv (3 - hlwb ntawm lub txiav (Karagezyan K.G., Gevorkyan D.M., 1989) , Litvinchuk M.M., 1994).

Lub tshuab kev txhim kho ntawm cov kab mob ntshav qab zib streptozotocin yog txuam nrog nws lub peev xwm los txo qis ntawm NAD, vim qhov nce ntawm cov haujlwm ntawm poly-ATP ribose synthetase (Yamoto N. et al., 1990), kev ua haujlwm ntawm lipid peroxidation, kev txo qis hauv kev ua haujlwm ntawm cov kab mob antioxidant thiab superoxide dismutase (Ovcharova N.I. et al., 1998). Kev qhia ntawm dithizone hauv kev sim tseem ua rau muaj kev txhim kho tsis muaj qhov tsis txaus siab, vim tias kev tsim cov khoom ua kom muaj kuab lom nrog zinc los ntawm dithizone nrog kev txhim kho ntawm cov txheej txheem puas tsuaj hauv (3 - hlwb ntawm islets ntawm Langerhans (Bayers JW, 1991). Kev ua kom muaj LP thiab kev nyuaj siab ntawm kev tiv thaiv antioxidant yog cov txheej txheem dav dav hauv kev txhim kho ntawm txhua qhov kev sim. qauv ntawm ntshav qab zib mellitus tsis yog tsuas yog 1, tab sis kuj ntawm hom: thaum pub cov nas qub nrog sucrose ntau dhau, kev txhim kho kev nyuaj siab oxidative hauv beta hlwb tau nthuav tawm (Yu I. et al., 1999).

Nws tau tsim tsa uas tsis tsuas yog hyperglycemia, tab sis kuj tseem hyperinsulinemia yog koom tes nrog cov txheej txheem ntawm kev nce siab oxidative hauv ntshav qab zib. (Balabolkin M.I., 2000). Nws yog qhov tseeb tias cov mob hyperglycemia los ntawm kev nce ntxiv ntawm tus nqi ntawm autooxidation ntawm cov piam thaj nce qhov kev tsim cov dawb radicals, nce glycosylation cov txheej txheem, ua rau muaj kev tsim cov oxidized ntau dhau ntawm cov protein, thiab cov dej num ntau ntxiv ntawm polyol pathose glucose metabolism ntxiv rau kev ua kom lub cev ntawm NADPH + khw muag khoom.Hyperinsulinemia ua kom muaj kev tiv thaiv kev mob hlwb thiab kev tsim cov dawb radicals los ntawm catecholamines, thiab los ntawm kev nce qib ntawm cov roj ntsha tsis sib luag los ntawm catecholamines tsub kom tsim cov dawb radicals thiab txo cov qib glutathione (ib qho tseem ceeb tshaj plaws ntawm dej-soluble antioxidants) (Balabolkin MI, Klebanova EM, 2000 )

Cov radicals dawb, tsis hais txog lub tshuab thiab cov peev txheej ntawm lawv tsim, ua rau qhov hloov pauv hloov Nf - kB, nrawm apoptosis thiab nce kev tsim cov oxidized qis-lipoproteins tsawg (LDL) (Demidova I.A. li al., 2000). Qhov kev hloov pauv ntawm Nf - kB ua lub luag haujlwm tseem ceeb - nws yog lub luag haujlwm rau ntau qhov kev cuam tshuam, tag nrho cov txiaj ntsig ntawm qhov ntawd yog qhov kev hloov pauv ntawm endothelium ntawm phab ntsa vascular. Qhov tseeb Nf-kB mediates qhov kev tso tawm ntawm cov qog necrosis factor a-interleukin-1P, uas yog koom nrog ntau cov txheej txheem uas ua rau tsis tsuas hloov ntawm phab ntsa vascular, tab sis kuj ua rau muaj qhov tsis txaus nyob rau hauv kev zais thiab kev ua ntawm insulin thiab ua rau lub siab tsis xws luag hlab hlwb (Shestakova M .V., Et al. 1996).

Yog li, nyob rau hauv cov ntshav qab zib mellitus, oxidative kev nyuaj siab yog nrog los ntawm kev nce ntxiv ntawm cov dawb radicals, uas, sib cuam tshuam nrog lipids, carbohydrates, thiab amino acids, hloov cov protein tsim cov khoom ua rau oxidation thawj thiab reactive carbonyl intermediates (carbonyl kev nyuaj siab). (Chernov, Yu.N., li al., 1998, Podoprigorova V.G., 2001).

1.2 .2. Cov nta ntawm lipid metabolism hauv cov ntshav qab zib mellitus, nws lub luag haujlwm hauv atherogenesis.

Tau ntev, ntshav qab zib tau suav tias tsuas yog kev ua txhaum ntawm cov metabolism hauv cov metabolism, thiab kev saib xyuas ntawm cov piam thaj tsis muaj peev xwm nyob hauv cov ntshav tau txiav txim siab tsuas yog cov tshuaj insulin (Laakso M., li al., 1998). Txawm li cas los xij, tam sim no pom tseeb tias tus kab mob no nrog cov kev cuam tshuam ntawm cov zaub mov tsis txaus siab ntawm tsis tsuas yog cov carbohydrates, tab sis kuj lipids thiab cov protein, thiab ob qho kev mob loj ntawm cov ntshav qab zib mellitus: atherosclerotic kev puas tsuaj rau cov hlab ntsha loj thiab ketoacidosis yog qhov tshwm sim ntawm lipid metabolism tsis txaus (Andrade S. E., et al., 1996).

Hauv cov neeg mob uas muaj ntshav qab zib hom, nrog tswj tau cov ntshav qabzib, lipid thiab ntshav siab nyob tau ntev li qub. Txawm li cas los xij, kev tswj xyuas cov kua nplaum tsis txaus thiab kev txhim kho cov qog ntshav muaj nrog rau cov ntshav dyslipidemia thiab arterial hypertension. (Doborgginidze JIM., Graziansky N.A., 2001).

Qhov kev pheej hmoo tseem ceeb tshaj plaws hauv kev kwv yees rau cov neeg mob ntshav qab zib yog dyslipidemia, uas yog yam ntxwv zoo thiab muaj txiaj ntsig hloov ntshav lipoproteins (Kozlov S.G. et al., 2000, Laasko M., 1995).

Cov yam ntxwv thiab cov cim ntawm dyslipidemia feem ntau ntawm cov neeg mob ntshav qab zib hom yog cov hauv qab no (Steiner G., 1994, Haffner SM, 1999): 1) kev nce qib ntawm triglycerides (TG) thiab qis kawg lipoproteins (VLDL), uas yog cov tseem ceeb ntawm cov neeg mob ntawm TG, 2) txo qis qib theem ntawm cov roj (cholesterol) ntawm cov "anti-atherogenic" feem - cov lipoproteins ntau ntom (HDL). Lub pathogenesis ntawm tus mob no yog qhov nyuaj thiab tuaj yeem "chiv" nyob rau ntau txoj hauv kev, txawm hais tias nws yuav ib txwm taug rau hyperinsulinemia vim insulin tsis kam thiab rog, uas feem ntau pom muaj ntshav qab zib (Howard V. V., 1995).

Insulin tsis kam ua rau cov lipolysis nce ntxiv thiab qhov kev tso tawm ntau ntawm cov roj ntsha dawb los ntawm adipose cov ntaub so ntswg, uas, ua ke nrog cov ntshav qabzib ntau ntxiv cov ntsiab lus, muab ib qho nyiaj ntxiv rau cov txheej txheem rau cov synthesis ntawm TG hauv lub siab (uas mus raws cov kab mob glycerophosphate). Raws li, muaj coob leej cov lipoproteins tsawg tsawg (VLDL) nplua nuj nyob hauv TG yog tsim ua ke (Yafasov K.M., Dubyanskaya N.V., 2001, Pierce L. R., li al., 1990, Herman W.H. li al., 1999).

Ntxiv nrog rau kev txhim kho cov synthesis ntawm VLDL, qhov kev ua txhaum ntawm catabolism ntawm cov lus no kuj tseem ceeb, vim qhov txo qis hauv kev ua haujlwm ntawm cov lipoprotein lipase nyob rau hauv cov ntshav qab zib, uas hydrolyzes TG, chylomyocrons thiab VLDL, uas ua rau kev tsim cov roj ntsha uas siv los ua lub zog rau cov leeg nqaij. (Taskinen M.R.1992, Baillie G. M., et al., 1998). Tag nrho cov no ua rau muaj kev nce ntxiv hauv cov lej ntawm lub cev, triglyceride-nplua nuj seem lipoprotein hais, uas yog suav hais tias yog tshwj xeeb tshaj yog atherogenic. Qhov kev sib xyaw ntawm HDL cov roj (cholesterol) tsawg dua vim muaj kev hloov pauv ntawm cov roj (cholesterol) esters los ntawm HDL rau VLDL thiab chylomyocrons hauv kev sib pauv rau triglycerides nyob hauv kev cuam tshuam ntawm cov protein uas hloov cov roj cholesterol esters (Stein EA, li al., 1998, Kozlov S.G., Lyakishev A .A., 1999, Feher MD, li al., 1995).

Lwm qhov kev tshwm sim ntawm kev ua txhaum ntawm lipid thiab lipoprotein spectrum ntawm cov ntshav yog qhov nce ntxiv ntawm cov me me, ntom LDL phenotype B, uas tau nce atherogenicity (Bakker - Arkema R.G., li al., 1996, Chapman M. J., li al., 1998). Qib ntawm apoprotein B yog qhov ntsuas uas muaj pes tsawg tus LDL hais, thiab cov roj cholesterol hauv LDL cov kab mob tuaj yeem sib txawv. Cov me me, ntom ntom ntawm LDL yog qhov loj dua qhov loj ntawm LDL (phenotype A), raug hloov los ntawm oxidative kev hloov kho thiab enzymatic glycosylation, uas qeeb lawv cov kev tshem tawm los ntawm ntshav (Chapman M.J., li al., 1998).

Thaum ua kev tshawb fawb txog kev mob sib kis hauv cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus, hypercholesterolemia vim qhov nce ntawm theem ntawm LDL cov roj cholesterol feem ntau tau pom. Raws li cov kev tshawb fawb ntau (Harris M.I., 1991, Baillie G.M., li al., 1998, Laasko M., li al., 1998), kev nce plasma plasma plob tsis txaus raug kuaj pom hauv 54-77% ntawm cov neeg mob.

Ib qho ntawm cov kev tshawb fawb tseem ceeb tshaj qhia qhov kev sib raug zoo ntawm qib ntawm tag nrho! rau cov roj ntshav thiab cov hlab plawv tuag hauv cov neeg mob ntshav qab zib mellitus yog Ntau Qhov Kev Ntsuam Xyuas Teeb Meem (MRFIT) (Stamler J., li al., 1999, Kannel W.B., li al., 1999). Nws cov txiaj ntsig tau qhia tias cov qib roj hauv lub siab ntau dua hauv tus neeg mob ntshav qab zib, muaj feem ntau ntawm cov kab mob plawv tuag. Nws tau pom tias nrog tib qib roj cholesterol, kev tuag ntawm cov neeg mob ntshav siab yog 3-4 npaug ntawm cov neeg mob ntshav qab zib ntau dua li qhov nws tsis tuaj. Qhov tseeb no qhia tau hais tias cov ntshav qab zib pab txhawb nqa ntau qhov kev pheej hmoo ntawm kev tuag los ntawm kab mob plawv rau lub cev ntxiv rau hypercholesterolemia.

Nrog rau qhov ntau, rau cov neeg mob ntshav qab zib, kev hloov pauv hauv lipoproteins yog qhov txawv txav, uas tuaj yeem ua rau lawv cov atherogenicity ntau zog (Feingold K.R., li al., 1992, Haffner, li al., 1994). Kev hloov pauv ntawm cov qauv ntawm lipoproteins, suav tias yog qhov tshwm sim ntawm kev txhim kho nrawm ntawm atherosclerosis hauv ntshav qab zib tuaj yeem tshwm sim los ntawm nonenzymatic glycosylation ntawm lawv cov apolipoproteins (Gurtis L.K., Witztum J.L., 1995). Glycosylation ncaj qha nyob ntawm theem ntawm cov piam thaj hauv cov ntshav thiab tshwm sim txij li pib ntawm ntshav qab zib. Apolipoproteins, uas yog ib feem ntawm cov chav kawm tseem ceeb ntawm lipoproteins, tuaj yeem hloov pauv cov txheej txheem, uas ua rau muaj kev hloov pauv hauv lawv cov metabolism, tshwj xeeb, kev nce qib hauv lub sijhawm ntawm VLDL (Witztum JL, li al., 1992) thiab LDL (Mamo JKL, li al., 1990) Cov. Txawm li cas los xij, qhov tseem ceeb tshaj plaws yog qhov txo qis hauv kev muaj peev xwm ntawm glycosylated LDL raug tshem tawm los ntawm cov hlab ntshav los ntawm lawv cov receptors. Qhov no ua rau qhov kev tshem tawm ntawm qhov tseem ceeb ntawm LDL hauv txoj kev tsis muaj kev txais: hloov kho LDL tau nrawm dua thiab yooj yim los ntawm macrophages nrog kev tsim cov npuas ua npuas, uas yog lub ntsiab lus tseem ceeb hauv pathogenesis ntawm atherosclerosis (Steinbrecher U.P. et al., 1993). Muaj pov thawj ntawm kev nce hauv platelet kev sib sau thaum raug rau glycosylated LDL (Bowie A, li al., 1993, Wolff S.P., Dean R.T., 1997).

Lwm qhov kev hloov kho zoo hauv lipoproteins hauv ntshav qab zib tuaj yeem tshwm sim los ntawm peroxidation, uas yog ib feem ntawm lawv cov lipids. Ib cov xov tooj ntawm cov ntawv tshaj tawm tau hais txog qhov theoretical prerequisites kom muaj lipid peroxidation ntau ntxiv hauv cov ntshav qab zib mellitus (Dedov II, li al., 2000, Kiahara M., li al., 1980, Hicks M., li al., 1998).

Kev rho tawm ntawm lipoproteins hloov kho rau hauv cov vascular phab ntsa nrog kev pab ntawm cov receptors uas tsim nyog, nrog rau cov chaw txais, ua rau tsis muaj kev sib txuam ntawm cov tom kawg hauv intima ntawm cov hlab ntsha, ua raws li kev tsim cov kev tiv thaiv kab mob ua ke ntawm Ig G, P - lipoproteins thiab ntxiv. Nws yuav tsum raug sau tseg tias macrophages xws li ntau lub chaw ntes tau nquag tshaj li haiv neeg ntshav lipoproteins (Serov V.V., 1998).Tsis tas li ntawd, macrophages txhawb kev nthuav qhia ntawm interleukin endotheliocytes rau ntawm daim nyias nyias; lawv qhib T-lymphocytes, uas nyeg tswj kev qhia ntawm E-selectin, intercellular thiab cellular nplaum lwg me me (ICAM-1, VACM-1), macrophage stimulating factor, interleukin-8, endothelin - 1, pab txhawb kev ua txhaum ntawm cov khoom nplaum, permeability ntawm lub ntsa ntsa thiab nws cov sclerosis (Saltykov BB, 2001). Macrophage ntau lawm ntawm cov qog necrosis ua rau muaj qhov nce ntxiv, uas txhim kho cov txheej txheem ntawm lipid peroxidation nrog kev tsim cov pa oxygen intermediates, txhawb txoj hauv kev arginine-tso rau ntawm kev tsim cov nitric oxide, thiab inhibits macrophages los ntawm kev nthuav qhia antigens rau T cell (Nagornev V.A. li al., 1999). Nyob rau tib lub sijhawm, kev zais cia ntawm lipoprotein lipase yog suppressed, kev hloov kho ntawm lipoproteins ntau ntxiv nrog lawv cov kev txuam nrog ntxiv hauv cov vascular phab ntsa. Lysophosphatidylcholine (LPH) yog lub hauv paus tseem ceeb ua rau oxidized LDL raug mob. Nyob hauv nws cov cawv, cov synthesis ntawm nitric oxide (N0) cuam tshuam, qib ntawm NOS-3 noob qhia raug txo qis, thiab kev ua haujlwm ntawm endothelial synthetase kuj tseem raug tswj (Zotova I.V. li al., 2002; Balakhonova T.V. et al., 2002) Cov.

Hypercholesterolemia kuj tseem yog lub zog tseem ceeb hauv atherogenesis, pab txhawb kev txhim kho ntawm endothelial kawg vim yog theem nrab inhibition ntawm endothelial synthetase los ntawm kev ua rau muaj kev qhia ntau ntawm cov neeg ua haujlwm ntawm Caveolin - (Kazuhino S. li al., 1997).

Hauv cov neeg mob ntshav qab zib mellitus, qhov nce ntxiv ntawm kev ua haujlwm ntawm intravascular ntawm platelets, qhov kev txo qis hauv qhov kev ua haujlwm antiplatelet ntawm vascular phab ntsa, ua rau muaj qhov tshwm sim ntawm platelet aggregates hauv vascular txaj thiab qhov tsis txaus microcirculation tau pom. Ib qho ntxiv, platelets tso platelet kev loj hlob tau, uas yog mitogen, thiab ua lub luag haujlwm tseem ceeb hauv kev txhim kho atherosclerosis los ntawm kev txhawb txoj kev loj hlob ntawm cov leeg hlwb thiab lawv tsiv teb tsaws los ntawm txheej nruab nrab ntawm cov hlab ntsha mus rau endothelium, thiab cov leeg nqaij mos yog qhov chaw ntawm cov txheej txheem sib txawv ntawm cov nqaij fibro-muscular plaque (Balabolkin M. I. et al., 2000). Ntxiv rau, kev mob ntshav qab zib microangiopathy vasa vasorum nrhiav pom (Saltykov D.D., 2002), nyeg, ua rau mob ntshav tawm, hloov pauv hauv cov hlab ntshav ntawm cov hlab ntsha loj, ua rau hypoxia, txhawb kev nce vascular permeability, ntshav impregnation nrog kev puas tsuaj rau phab ntsa ntawm cov hlab ntsha thiab kev txhim kho ntawm atherosclerosis.

1.3 Cov teeb meem thiab kev cia siab ntawm kev siv tshuaj kho mob ntawm cov neeg mob ntshav qab zib mellitus.

Pharmacotherapy ntawm cov ntshav qab zib mellitus yog txoj haujlwm kho mob nyuaj, hauv kev daws teeb meem uas nws yog ib qho tsim nyog yuav tsum coj mus rau hauv tus account cov yam ntxwv ntawm kev txhim kho ntawm cov txheej txheem pathological.

LEEJ TWG tau tshaj tawm cov ntshav qab zib yog ib qho kev sib kis ntawm cov kab mob sib kis tsis tau, txhua txhua 10-15 xyoo tus naj npawb ntawm cov neeg mob ntshav qab zib muaj ntau dua (Dedov I.I., 2000). Microvascular cov teeb meem ntshav qab zib tseem yog cov teeb meem tseem ceeb ntawm cov kab mob ntshav qab zib soj ntsuam, kev nthuav dav ntawm angiopathy hauv cov neeg mob ntshav qab zib yog 90-97%. Mob ntshav qab zib retinopathy thiab neuropathy, nrog rau visceral thiab peripheral polyneuropathy, yog qhov tseem ceeb ntawm kev tsis taus thiab kev tuag ntawm cov neeg mob (Bobyreva JI. E., li al., 2000).

Atherosclerosis nyob rau hauv cov neeg mob ntshav qab zib mellitus yog tus cwj pwm los ntawm kev txhim kho thaum ntxov thiab kev kis tus kab mob, uas tso cai rau peb hais txog ntshav qab zib ua ib qho qauv ntawm atherosclerosis (Kovaleva P.V., 2002).

Kev kuaj ntshav qab zib yog txiav txim siab los ntawm lub sijhawm ntawm qhov pom ntawm angiopathy thiab mob hnyav. Kev mob ntshav qab zib yog qhov ua rau muaj kev tuag nyob rau hauv tsis ntau tshaj 1-2% ntawm cov neeg mob, thaum lub sijhawm uas tuag los ntawm cov neeg mob ntshav nce mus txog 65-80% (Fadeeva NI, 2001).

Mob ntshav qab zib mellitus thiab cov kab mob plawv ua ke. Hauv ntau dua 60% ntawm cov neeg mob ntshav qab zib, lub neej cia siab muaj tsawg tsawg los ntawm cov kab mob txhim kho plawv sai heev (Karpov, Yu.A., 2002).

Muaj cov ntshav qab zib nce ntau zaus ntawm kev tuag sai rau cov txiv neej los ntawm 50% thiab hauv cov poj niam los ntawm 300% (IDE, 2000). Nws yog ib qho tseem ceeb tias kev soj ntsuam ntawm cov neeg mob ntshav qab zib mellitus uas tsis muaj mob rau cov hlab ntshav yog kwv yees li qhov qub rau cov neeg mob uas muaj mob ntshav txhaws tsis muaj ntshav qab zib.Coj los ntawm cov lus tseeb no, American Heart Association tau faib cov ntshav qab zib yog cov kab mob ntawm cov hlab plawv (Karpov, Yu.A., 2002).

Cov kev pheej hmoo tseem ceeb rau kev txhim kho thiab kev loj hlob ntawm cov mob ntshav qab zib ua mob ntshav qab zib yog hyperglycemia, arterial hypertension thiab dyslipidemia (Shestakova M.V., 2002). Yog li, qhov nce ntawm glycated hemoglobin los ntawm 6% mus rau 10% ua rau muaj qhov nce ntawm cov zaus myocardial infarction hauv cov neeg mob uas muaj ntshav qab zib hom 2 los ntawm 2,5 zaug (UKPDS, 2000). Ib qho kev nce ntxiv hauv cov ntshav roj ntau los ntawm mus rau mmol / L 2.5 lub sij hawm ua rau kev tuag ntawm cov neeg mob ntshav qab zib mellitus los ntawm kev mob plawv (MRFIT, 2000).

Txawm tias muaj kev nce qib hauv kev soj ntsuam txog tus kab mob ntshav qab zib niaj hnub no, kev mus sij hawm ntev ntawm kev kho mob ntawm cov neeg mob tseem nyob tsis txaus siab. Thaum lub xyoo tsis ntev los no, hauv ntau lub tebchaws, kev tuag los ntawm cov kab mob plawv tau poob qis yuav luag ob zaug (Aronov D.M., 2001), tom qab ntawd hauv cov tebchaws no kev tuag los ntawm kab mob plawv tsis tau hloov pauv hauv pab pawg ntawm cov neeg mob ntshav qab zib mellitus, tab sis cov poj niam txawm tias nce (Shestakova M.V., 2000, Gu K. et al., 1999, DCST, UKPDS, 2000).

Txog rau hnub no, ntau cov lus nug tseem tsis tau daws txog kev kho cov teeb meem hauv cov ntshav qab zib mellitus.

Kev siv cov kev tiv thaiv hypoglycemic hauv kev xyaum ua rau qhov teebmeem nyuaj dua, tam sim no tau daws nrog kev pab ntawm kev noj zaub mov kom lub cev tsis zoo, kev ua kom lub cev, qhov ncauj qab zib kom qis tshuaj (sulfonylurea derivatives thiab guanine-biguanides) thiab insulin. Txawm li cas los xij, tsis muaj ib txoj hauv kev los kho cov hyperglycemia muaj txiaj ntsig zoo dua li lwm tus: nrog lawv siv kom raug, qhov tshwm sim ntawm myocardial infarction hauv cov neeg mob uas muaj ntshav qab zib mellitus tsawg dua 16% (UPDAS, 1998). Tam sim no, tshuaj sulfanilamide yog lub pob zeb nyob hauv kev txo qis qab zib. Qhov kev txaus siab hauv pab pawg ntawm cov tebchaw no tau piav qhia los ntawm qhov tseeb tias lawv tsuas yog chav kawm ntawm hypoglycemic tshuaj uas muaj lawv tus kheej receptor ntawm lub plasma membrane (3-hlwb (Ashcroft FM li al., 1998). ua rau depolarization ntawm lub plasma membrane, qhib kev siv hluav taws xob-calcium calcium raws thiab qhov nce ntawm cov tshuaj tua kab mob calcium uas tsis txaus, uas, los ntawm khi rau calmodulin, ua kom muaj zog insulin exocytosis (Aschcroft FM, 1996, Kramer W. et al., 19) 99) Txawm hais tias muaj ntau hom tshuaj sulfanilamide, qhov kev xaiv ntawm cov tshuaj los txo cov hyperglycemia feem ntau tau txwv ntau vim tias muaj qhov tshwm sim ntau ntawm kev txhim kho ntawm ntau cov kev mob tshwm sim.Thaum noj sulfanilamides, kev txo qis hauv hyperglycemia yog pom tsuas yog hauv 70-75% ntawm cov neeg mob, thiab yog tias muaj kev kho mob tshuaj. Cov nyhuv ntawm qhov tshwm sim uas nquag thiab loj tshaj plaws yog cov ntshav qab zib thiab hypoglycemic coma (Coop LC, 1998, Holman RR, Turner RC, 1999). Hauv 35% ntawm cov neeg mob kho nrog sulfonamides, tiv thaiv sulfanilamide theem pib loj dua txhua xyoo.

Ntev mus kuaj ntawm pancreatic P - hlwb tuaj yeem ua rau lawv cov kev ua kom tiav sai thiab ntau tshaj tawm cov insulin tsis txaus, nrog rau kev zais kev tsis txaus los ntawm qog proinsulin thiab splitproinsulin hlwb, uas ua rau muaj kev pheej hmoo ntawm atherogenesis (Alexandrov A. A., 2001, Ohkubo Y. et al., 1995, Turner RC, 1999). Tsis tas li ntawd, qhov tsis zoo tshwm sim ntawm sulfonylurea kev npaj rau ntawm kev mob plawv hauv cov neeg mob uas muaj ntshav qab zib hom tau raug qhia tawm. Hauv pawg ntawm cov neeg mob tau txais tolbutamide, kev tuag ntawm myocardial infarction yog 50%, thaum nyob hauv pawg nrog placebo 18% (Engler R., 1996). Cov txiaj ntsig tsis zoo ntawm sulfonamides nyob rau ntawm chav kawm thiab kev mob ntshav siab hauv lub plawv rau cov neeg mob ntshav qab zib mellitus yog vim lawv lub peev xwm los tiv thaiv ATP-dependant potassium nyob rau hauv myocardium, du thiab pob txha nqaij, thiab qee cov hlwb hlwb (Aschcroft F.M., 1999).Nws ntseeg tias Kahf channel yog qhov tsim nyog rau kev ua kom tiav cov txheej txheem ntawm cov metabolism hauv intracellular thiab kev zoo siab ntawm lub plasma membrane, zoo li rau kev paub tseeb txog qee yam kev cuam tshuam ntawm qee cov tshuaj hormones thiab cov tshuaj lom biologically active thiab kev tswj hwm vascular.

Nicols C.G., 1991, Aschcrofit F.M., Reiman F., 2000). Kev ua kom muaj cov poov tshuaj tso tawm muaj cov txiaj ntsig cardioprotective hauv myocardial ischemia (Escande D., li al., 1992). Cov tsim tawm ntawm sulfonylureas tshuaj xyuas cov teebmeem no, yog li, muaj kev phom sij nrog kev sib txuam ntawm ischemic mob plawv thiab ntshav qab zib. Qhov yuav tshwm sim ntawm kev siv tshuaj sulfa tuaj yeem ua rau ua xua lossis tshuaj lom (tawv nqaij ua kom khaus, urticaria, Quincke's edema, leukopenia, granulocytopenia, thrombocytopenia, hypochromic anemia), tsis tshua muaj tsos mob dyspeptic (xeev siab, mob rau thaj tsam epigastric, ntuav). Qee zaum muaj kev ua txhaum lub siab nyob rau hauv daim ntawv ntawm lub ntsej muag daj vim cholestasis (Gorbenko NI, 1999).

Cov pab pawg thib ob ntawm qhov ncauj hypoglycemic yog biguanides, uas txo hyperglycemia nyob rau hauv cov neeg mob ntshav qab zib mellitus los ntawm kev txhim kho qhov rhiab ntawm daim siab thiab peripheral cov ntaub so ntswg rau insulin tsis muaj kev cuam tshuam lub zais ntawm cov tshuaj hormones (Dunn C.D., Peters D.H., 1995, Perriello G., 1995). Biguanides tau suav hais tias yog cov tshuaj ntawm thawj qhov kev xaiv hauv kev kho mob ntawm cov neeg mob rog uas muaj hom thiab / lossis ntshav qab zib nrog lub cev tsis muaj ntshav thaum pib ua kev kho mob lossis ua ke nrog cov tshuaj sulfonamide (Balabolkin M.I. et al., 2001, Dunn C.D., 1995).

Ib qho kev mob tshwm sim ntawm biguanides yog qhia nyob rau hauv lactic acidosis, kev ua xua ntawm daim tawv nqaij, cov tsos mob dyspeptic (xeev siab, tsis xis nyob hauv plab thiab mob plab), exacerbation ntawm tus mob ntshav qab zib polyneuropathy (vim tias qhov txo qis ntawm kev nqus ntawm cov vitamin B12 hauv plab hnyuv me) (Chernov, Yu.M. et al. ., 1999).

Ib txwm siv nyob rau hauv cov ntshav qab zib mellitus, kev kho tshuaj insulin kuj muaj ib tug xov tooj ntawm cov teeb meem daws tsis tau. Kev kho mob siab tshaj plaws nrog insulin tuaj yeem txo qhov kev pheej hmoo ntawm kev mob ntshav qab zib, txawm li cas los xij, kev noj tshuaj ntev ntev ntawm cov tshuaj insulin ua rau hyperlipidemia, ua rau muaj kev pheej hmoo ntawm atherosclerosis los ntawm ntau zaus (E. Krasilnikova li al., 1996). Kev siv cov tshuaj insulin yog nrog los ntawm kev txhim kho cov teeb meem uas tsis tsuas yog ua rau lub neej tsis zoo ntawm cov neeg mob ntshav qab zib mellitus, tab sis kuj tseem ua rau cov xwm txheej tsis zoo rau tus neeg mob lub neej. Cov no suav nrog: hypoglycemia, posthypoglycemic hyperglycemia (Somogy tshwm sim), kev tsis haum tshuaj, kev tawm tsam insulin, kev txhaj tshuaj tiv thaiv kab mob insulin lipodystrophies, insulin edema, tsis pom kev (Balabolkin MI, 2000). Qhov tsis zoo ntawm cov tshuaj insulin kuj tseem yog qhov kev hloov pauv ntawm kev tswj hwm, uas, ntxiv rau qhov tsis yooj yim rau tus neeg mob, muaj feem xyuam nrog pharmacokinetics ntawm insulin npaj: insulin, muab tshuaj subcutaneously, nkag mus rau hauv cov hlab xa hluav taws xob sai dua li ncaj qha rau daim siab los ntawm lub vev xaib vein, zoo li hauv kev mob physiological (Saudek CD, 1997 )

Yog li, cov txiaj ntsig tsis txaus siab ntawm kev siv cov tshuaj lom neeg ib txwm nyob, nrog kev pheej hmoo siab ntawm cov kev mob tshwm sim, qhov nce sai ntawm cov teeb meem vascular thiab cov txiaj ntsig tuag taus txawm tias thaum kho, hais txog qhov xav tau los tsim cov tshiab, tsis tshua muaj kev phom sij thiab muaj txiaj ntsig zoo dua ntawm cov tshuaj los kho cov teeb meem hauv cov ntshav qab zib mellitus (Campbell RK, 1999).

Cov kev tshawb fawb tsis ntev los no tau qhia (Perova N.V. et al., 2001, Heinemann L. et al., 1997, Hoffman A., 1999) kev saib xyuas ntawm cov teeb meem pheej hmoo ntau dua, muaj ntau qhov ua tau zoo tshaj qhov kev cuam tshuam ntawm cov metabolism hauv ntshav qab zib mellitus thiab txhim kho kev soj ntsuam rau lub neej nyob rau hauv cov neeg mob ntawd.

Raws li ib feem ntawm cov metabolic syndrome, cov neeg mob ntshav qab zib mellitus feem ntau muaj dyslipidemia, arterial tawg thiab rog, uas yog ywj pheej txog kev pheej hmoo rau cov kab mob plawv uas yuav tsum tau kho.

Feem ntau thoob plaws hauv lub ntiaj teb ntawm cov txhais tau tias tsom mus kho kho dyslipidemia nyob rau hauv ntshav qab zib mellitus yog statins lossis inhibitors ntawm 3-hydroxy-3-methylglutaryl-coenzyme A-reductase. Cov tshuaj no thaiv kev sib txuas ntawm ib qho enzyme uas ua kom nrawm tsim cov roj (cholesterol) hauv lub siab (Shestakova M.V., 1999).Qhov ua tau zoo ntawm cov tshuaj statins tau pov thawj pom nyob hauv ntau qhov kev tshawb fawb ntau yam (Mellies M.J., 1993). Ib qho ntawm cov kev tshawb fawb no, 4s, tau mob siab rau txoj kev kawm ntawm kev muaj sia nyob ntawm cov neeg mob uas muaj mob ua mob rau lub cev thaum txoj kev kho mob nrog Zocor. Txoj kev tshawb no tau siv sijhawm ntev dua ntau xyoo, nws koom nrog 4444 cov neeg mob hypercholesterolemia thiab mob plawv, ntawm cov neeg mob ntshav qab zib mellitus (Pyorala K. li al., 1997). Tom qab lub lim piam ntawm kev kho mob nrog Zocor ntawm koob tshuaj 20 mg / hnub hauv cov neeg mob ntshav qab zib, qhov kev txo qis hauv cov ntshav roj tag nrho yog 28%, HDL cov cholesterol los ntawm 37%, TG los ntawm 18% thiab nce HDL cov cholesterol los ntawm 8% tau sau tseg. Hauv qib no, cov nyhuv tau kav ntev rau xyoo kho.

Txawm li cas los xij, kev siv mus ntev li ntev tau los tiv thaiv cov kev ua si ntawm ib qho ntawm antioxidant enzymes Qi0 hauv lub siab, uas ua rau muaj kev pheej hmoo ntawm cov txheej txheem LPO ntau ntxiv (V. Lankin, 2000). Tsis tas li ntawd, ntawm cov neeg mob koom nrog cov kev tshawb fawb, tsis muaj ib tus neeg twg uas muaj tus kab mob siab triglycerides ntau, yog li lawv cov txiaj ntsig tsis tuaj yeem txuas rau tag nrho cov pej xeem ntawm cov neeg mob uas muaj mob plawv.

Hauv qhov no, fibrates, uas nquag cuam tshuam rau theem ntawm triglycerides, tuaj yeem ua cov tshuaj uas xaiv. Qhov tshwm sim ntawm cov fibrates ntawm cov ntshav lipids yog nrog los ntawm kev txo qis hauv qhov LDL ntom, thiab, yog li ntawd, qhov txo qis ntawm cov tshuaj atherogenic me me ntom LDL (Kozlov S.G. li al., 1999). Nws yog qhia tias nrog kev siv ntev ntev ntawm hemofibrozil, qhov kev tuag ntawm cov neeg mob ntshav qab zib los ntawm kab mob plawv yog nce li 22%. Txawm li cas los xij, kev siv ntau ntawm cov tshuaj ntawm cov pab pawg no muaj kev txwv los ntawm ntau cov kev sib txuam thiab cov kev mob tshwm sim, suav nrog cholelithiasis, kev nce siab hauv cov roj (cholesterol), kev nce siab hauv transaminase kev ua si, xeev siab, myalgia, pob txha mob hypoplasia, leukopenia, thrombocytopenia, kev txhim kho cataracts, arrhythmias (Frishman W.H., 1995).

Nicotinic acid muaj cov nyhuv zoo li cov fibrates ntawm lipid profile tsis. Muaj pov thawj ntawm kev txheeb xyuas kev nyab xeeb ntawm kev sib xyaw ntawm nicotinic acid nrog simvastatin hauv cov neeg mob uas muaj cov roj (cholesterol) HDL tsawg thiab cov txiaj ntsig tau zoo ntawm qhov kev sib xyaw no thaum lub sij hawm ntawm lub plawv mob atherosclerosis (Gustafsson I. et al., 2000). Txawm li cas los xij, kev siv mus sij hawm ntev tsis tuaj yeem pom zoo vim qhov ua tau ntawm kev ua tsis zoo glycemic tswj, ua rau cov tshuaj tiv thaiv insulin tsis zoo thiab ua rau kev ua haujlwm ntawm lub zog kinin ntau dhau (Mikhaylyuk IB, 1998, Perova N.V. et al., 2001, Heinemann L. li al. Xyoo 1997, Hoffman A., 1999).

Kev tswj ntshav siab yog lwm txoj haujlwm tseem ceeb hauv kev kho mob rau cov neeg mob ntshav qab zib. Tus neeg mob coob coob hauv cov chaw kho mob tau hais tawm txog txoj kev ntshav siab ntawm cov neeg mob uas muaj ntshav qab zib hom 2 mus txog 70% (Karpov Yu.A., 2001).

Kev qhia ncaj qha los tiv thaiv tus mob ntshav qab zib mellitus yog sawv cev los ntawm: (3 - blockers, Ca antagonists thiab nitrates. Hauv Coteborg thiab MIAMI cov kev tshawb fawb, kev kho mob nrog P - blockers hauv ntshav qab zib mellitus ua rau txo qis kev tuag hauv ntau dua 3 lub hlis los ntawm 49-59%). mob ntshav qab zib yog cov teeb meem hauv lub cev vim ischemia muaj kev phom sij ntau dua vim yog hloov mus rau lub zog ntawm cov roj ntsha hauv lub cev myocardium, uas yog ib qho tshwm sim ntawm cov kev mob tshwm sim hauv lub cev, ua rau kev tawm ntawm glycol a, lactate tsub zuj zuj thiab ionic tsis txaus (American Diabetes Association, 1993) Qhov kev tshawb pom TRIMPOL-1 qhia tau tias kev ntxiv ntawm trimetazidine (kev tawm tsam), ib cov tshuaj nrog cov metabolic mechanism ntawm kev ua rau monotherapy nrog tshuaj tiv thaiv antianginal, txhim kho kev ua tau zoo thiab muaj txiaj ntsig zoo ntawm kev saib taus thiab cov tsos mob ntawm tus kab mob hauv 50% ntawm cov neeg mob ntshav qab zib mellitus. Txuas ntxiv rau kev ncua sijhawm ntawm kev ntsuas nrog kev ua si thiab kev txhim kho lub neej zoo, trimedazidine txo cov ntsiab lus ntawm von Willeb factor. randa (cim ntawm endothelial puas tsuaj) nyob rau hauv cov ntshav ntshav.

Nyob rau hauv xyoo tas los no, ntau lub ntsiab lus tau them mus rau kev txhim kho ntawm chav kawm tshiab ntawm cov tshuaj tiv thaiv kab mob - thiazolidinedione derivatives (troglitazone, rosiglitazone) (Saltiel A.R. et al., 1996). Cov tshuaj hauv cov pab pawg no khi rau lub a - subtype ntawm activated peroxisomal proliferator receptor (PPARy), ua rau muaj kev txhim kho hauv insulin rhiab heev thiab txo qis hauv cov tshuaj tiv thaiv hormone (Lebovitz N.E.).li al., 2000). Kev sim ua thiab kev soj ntsuam tau pom tias thiazolidinediones tuaj yeem ua kom nrawm rau kev siv cov kua nplaum los ntawm cov ntaub so ntswg los ntawm kev nce glycogen synthetase kev ua haujlwm thiab inhibit gluconeogenesis hauv daim siab, uas ua rau txo qis ntshav plasma. Tsis tas li ntawd, thaum kho nrog thiazolidinediones, qhov txo qis ntawm triglyceride concentration thiab ntshav siab, nrog rau kev rov qab los ntawm cov txheej txheem atherosclerotic (Sjostrom L. et al., 1998) tau sau tseg. Txawm li cas los xij, kev nthuav qhia dav dav ntawm cov tshuaj ntawm cov pab pawg no yog txwv los ntawm kev pheej hmoo siab ua rau lub siab puas tsuaj thiab kev txhim kho lub pob zais ntshav thiab mob hepatocellular mob siab rau cov neeg mob ntshav qab zib mellitus (Yasuki I., 2000, Riskin F. et al., 2000), ntxiv rau qhov muaj peev xwm txo qis cov qe ntshav liab thiab hemoglobin vim yog kev ntxhov siab nquag ntawm lub hlwb (Lebovitz N.E. et al., 2000).

Hauv kev muab tshuaj kho mob ntshav qab zib mellitus, txhawm rau txo cov teeb meem metabolism, kev siv cov tshuaj uas txwv cov glycosylation txheej txheem yog pathogenetically justified. Ib qho tshwj xeeb glycosylation inhibitor yog aminoguanidine (pimagedin), lub tshuab ntawm kev coj ntawm uas yog kom muaj kev cuam tshuam nrog Amadori cov khoom thiab kev tsim cov tshuaj lom neeg lub cev tsis sib luag hauv cov protein molecule (Edelstein D. et al, 1992, Zimmerman G.A. et al., 1995).

Kev txwv tsis pub muaj cov enzymatic glycosylation ntawm cov protein thiab oxidation ntawm qis lipoproteins yog tau siv cov tshiab potassium channel blocker AL 0671 (Yamauchi Takeshi li al., 1996, Engerman RL thiab Kern TS, 1996, Yasanari Kenichi li al., 1998, Sjostrom L. li al., 1998 1998).

Txhawm rau rov qab kho microcirculation thiab ib txwm ua ib qho kev nce ntxiv los tsim nthuav tawm ntawm kev mob sib kis ntawm cov nqaij mos, uas tau pom tias muaj ntau qib nyob rau hauv yuav luag txhua tus neeg mob ntshav qab zib mellitus, prostaglandins inhibitors (acetylsalicylic acid, thiab lwm yam) thiab thromboxane synthesis inhibitor -ibustrin yog siv (Shestakova M.V. , 2000), tsis tshua muaj molecular hnyav heparin, fraxiparin (Savenkov M.P. et al., 1999).

Kev cia siab loj tam sim no nyob rau hauv kev kho cov kab mob angiopathy hauv ntshav qab zib mellitus tau muab tso rau ntawm kev siv ACE inhibitors. Kev npaj ntawm cov pab pawg no muaj txiaj ntsig zoo rau kev kawm txog vascular pathology hauv cov neeg mob ntshav qab zib mellitus, kho myocardial kho nyob rau hauv cov hlab plawv, tiv thaiv kev txhim kho thiab kev loj hlob ntawm cov ntshav qab zib nephropathy, thiab qeeb cov kev vam meej ntawm kev pib mob hlwb (Rayaz A.S., 2000). Noj ramipril hauv cov neeg mob ntshav qab zib txo txoj kev pheej hmoo ntawm myocardial infarction los ntawm 22%, cerebrovascular kev sib tsoo los ntawm 33%, thiab kev pheej hmoo ntawm kev tuag los ntawm cov kab mob plawv los ntawm 37% (Chugunova JI.A. li al., 1999, Fuhlendorff J. et al, 2000 , Viraly ML, 2000).

Yog li, kev txheeb xyuas cov saum toj no, peb tuaj yeem xaus tias kev pheej hmoo ntawm kev phiv hauv cov ntshav qab zib mellitus yog qhov siab vim qhov peculiarities ntawm pathogenesis ntawm tus kab mob, muaj ntau cov kab mob hloov khoom nruab nrog, kev koom tes ntawm kev tshem tawm plab hnyuv siab raum thiab biotransformation ntawm cov tshuaj hauv cov txheej txheem pathological. Sim los cuam tshuam rau txhua qhov txuas ntau ntawm pathogenesis, tus kws kho mob, hmoov tsis, yog inexorably kos rau hauv polypharmacy. Hauv qhov no, nws tuaj yeem sib cav hais tias hauv kev kho mob rau cov neeg mob ntshav qab zib mellitus, nws yuav tsum tsim kho txoj hauv kev los saib xyuas lub xeev ntawm kev siv lub cev zom zaub mov, tshuaj xyuas cov cim ntawm cov tshuaj tiv thaiv peroxide thiab cov tshuaj tiv thaiv kab mob, uas yuav tso cai rau tus neeg xaiv thiab tswj kev kho mob thiab yuav pab kom ua tiav lub hom phiaj tseem ceeb - nce lub sijhawm thiab muaj lub neej zoo ntawm cov neeg mob.

1.4. Lub meej mom rau kev siv tshuaj tiv thaiv antioxidant hauv kev kho mob ntshav qab zib.

Hauv cov kab mob ntshav qab zib, kev paub tau nce nrog kev siv cov tshuaj tua kab mob ntau. Lub hauv paus, kev teem caij ntawm kev siv tshuaj tua kab mob rau kev mob ntshav qab zib tuaj yeem muaj ob lub hom phiaj: tiv thaiv (qeeb qis) kev txhim kho kabmob, tiv thaiv (maj mam poob) kev txhim kho ntawm nws cov teeb meem.

Soj ntsuam kev sim ntawm nicotinamide nyob rau hauv cov neeg mob nrog hom I debut tau ua txij thaum nruab nrab-80s.Nws tau qhia tias kev siv ntau ntawm cov tshuaj (kaum lub sijhawm ntau dua li lub zog ntawm lub cev) tiv thaiv qhov poob qis hauv kev ua haujlwm ntawm P - hlwb, raws li tuaj yeem txiav txim siab los ntawm theem ntawm basal thiab txhawb C-peptide (Gorelysheva V.A. li al., 1996, Kolb N. li al., 1999, Pozzilli li al., 1999). Raws li ob peb tus kws sau ntawv (Bondar I.A. et al., 2001, Hoorens A. et al., 1999, Kolb N. et al., 1999, Nerup J., 2000), kev kho mob nicotinamide ua rau muaj kev nce ntau hauv cov zaus kho mob. cov kab mob nrog kev xav tau qis rau cov kab mob muaj zog txaus (Visalli N., li al., 1999, Greenbaum C.J., 1996) a - Tocopherol yog dawb radical scavenger thiab lub ntsiab antioxidant ntawm membrane qauv: ib qho ntawm nws cov molecules tiv thaiv txog 10,000 tsis muaj roj fatty molecules. kua qaub. Cov txiaj ntsig kev tiv thaiv ntawm a - tocopherol (15 mg / kg ib hnub) ntawm kev ua haujlwm ntawm P hlwb yog ze rau qhov ntawm nicotinamide (25 mg / kg ib hnub) (Pozzilli P. et al., 1997). Hauv kev tshawb tshuaj vitro thiab tsiaj, nws tau pom tias a - tocopherol txo qhov ua rau endothelial ua rau los ntawm hyperglycemia, tiv thaiv kev ua haujlwm ntau dhau ntawm soluble adhesion molecules thiab txhim kho kev tsim cov tshuaj endothelial so (nitric oxide - TSIS TAU) (Frei B., 1999, Cowa D. et al., 1997, Bursell SE li al., 1999, Emmert DM li al., 1999).

Kev tshawb nrhiav CHAOS tau pom tias kev kho vitamin E ntawm ib koob lossis ME / hnub ua rau muaj kev txo qis (los ntawm 66%) hauv qhov tshwm sim ntawm qhov mob tsis muaj ntshav qab zib myocardial infarction hauv cov neeg mob uas muaj lub plawv mob rau lub plawv atherosclerosis, tab sis tsis yog nrog txo qis los ntawm kev tuag ntawm kev mob plawv (Stephens NG et) al., 1996).

Kev coj ua haujlwm tsis tu ncua ntawm lub voj voog ntawm cov vitamins E thiab C yog ua tau tsuas yog muaj nyiaj txaus ntawm lipoic acid hauv lub cev. (Balabolkin M.I. et al., 2000). Ntxiv mus, nws tau qhia tias tom qab kev sib cuam tshuam ntawm cov tshuaj insulin nrog nws cov receptor rau kev sib pauv ntawm cov kev mob lom ntawm insulin, qhov muaj cov lipoic acid yog qhov tsim nyog. Lipoic acid yog nthuav tawm raws li cofactor nyob rau hauv ntau cov enzyme complexes, yog lub "huv" ntawm cov dawb radicals, thiab kuj tseem pab kom rov ua lwm yam antioxidant hauv lub cev. Nws muaj cov txiaj ntsig tiv thaiv thiab tiv thaiv DNA ua puas los ntawm cov dawb radicals: nws inhibits kev ua haujlwm ntawm qhov teeb meem transcription Nf-kB tshwm sim los ntawm oxidative kev nyuaj siab, yog hlau chelator - Co, Cu, Cd, Ni, Zn, Raws li, Fe, Mg thiab ua cov khoom siv hu ua complexon (Bababolkin M. Thiab li al.,

Xyoo 2000, Perova N.V. et al., 2001, Okovitiy S.M. et al., 2002, Halliwell, W., 2000).

Cov ntaub ntawv tau los ntawm kev ua haujlwm ntawm selenium nyob rau hauv kev tiv thaiv ntawm nephropathy nyob rau hauv cov nas nrog cov ntshav qab zib hom 2 ua los ntawm streptozotocin. Cov nyhuv hypoglycemic ntawm selenium tau tshaj tawm dua thaum siv ua ke nrog vitamin E. Selenium txo qis lossis ib txwm muaj qhov nce ntawm arachidonic acid nyob rau hauv ob lub raum nrog cov ntshav qab zib, thiab txo cov zaus thiab qhov mob ntawm morphological pauv (Christelec D. et al., 1999).

Zelinsky B.A. li al. nyob rau xyoo 1994, tau qhia tias kev koom ua ke ntawm unitiol hauv txoj kev kho mob nyuaj rau cov neeg mob nrog kev sib xyaw ntawm cov pa oxygen thiab tocopherol muaj cov lus tshaj tawm zoo rau phospholipid metabolism ntawm ob qho ntshav ntshav thiab cov ntshav liab, pab ua kom lub cev cell thiab txhim kho nws txoj haujlwm. Thiab kev qhia txog kev qhuas hauv kev sib xyaw ua ke nrog cov tshuaj tiv thaiv kab mob rau cov neeg mob vascular mob ntshav qab zib, raws li cov ntsiab lus ntawm II. Dedova (1998) et al., Muaj kev tiv thaiv kev nyob ruaj khov ntawm txoj kev hauv ntau tshaj ib nrab ntawm kev tshuaj xyuas cov neeg mob. Phenolic antioxidants ionol thiab probucol pom tias lub peev xwm los ua kom lub ntsej muag hloov pauv zoo li tau pom nyob hauv ntshav qab zib alloxan (Bobyreva L.E., 1997, Tikhase A.K. et al., 1999).

Xyoo tsis ntev los no, cov kws tshawb nrhiav thiab cov kws kho mob tau nce siab txaus siab rau pab pawg ntawm cov dej-soluble antioxidants, uas suav nrog cov derivatives ntawm 3-hydroxypyridine, uas tuaj yeem ua rau ntau qhov txuas ntawm pathogenesis ntawm ntshav qab zib mellitus. Ob peb cov kev tshawb fawb, cov uas kev tshawb fawb ntawm A.A. Nelaeva thiab E.A. Kashuba pom tias kev siv emoxipin hauv cov neeg mob ntshav qab zib mellitus nrog angiopathy muaj cov tshuaj antioxidant, ua kom lub ntsej muag ua kom lub zog ruaj khov, thaum nws txo qis ntau zaus ntawm cov teeb meem vascular hloov hauv cov neeg mob.Qhov no qhia tau tias 3-hydroxypyridine derivatives muaj cov tshuaj tiv thaiv kev muaj peev xwm ua tau. Txawm li cas los xij, cov kev teeb tsa no tau kawm txog kev txom nyem heev los txog niaj hnub no. Peb pom zoo tias cov tshuaj no muaj cov kev cuam tshuam txhim kho ntawm cov kab mob sib kis kab mob ntshav qab zib mellitus thiab nws cov kev mob tshwm sim, raws li cov ntaub ntawv muaj nyob rau pharmacological cuam tshuam rau cov qauv ntawm lwm cov kab mob pathological.

1. Qhov cuam tshuam ntawm derivatives ntawm 3-hydroxypyridine ntawm lipid peroxidation thiab lub xeev ntawm cov cell nyias.

Mexidol (3-hydroxy-6-methyl-2-ethyl pyridine succinate) yog qhov muaj zog inhibitor ntawm cov txheej txheem LPO, nruab nrab cov radicals dawb, ua rau superoxide dismutase, hloov kho lub cev ntawm lub cev puas, ua rau cov ntsiab lus ntawm polar lipid feem ntau (phosphatidylserine thiab phosphatidylinositis). , txo cov viscosity ntawm daim nyias nyias, nce nws fluidity (Lukyanova L.D., 1999, 2000). Vim kev hloov pauv ntawm lub xeev ua haujlwm ntawm cov qog ua rau me me, mexidol ua rau muaj kev hloov pauv hauv cov macromolecules ntawm cov nqaijrog, synapses, uas yog qhov laj thawj ntawm cov txiaj ntsig mexidol ntawm kev ua haujlwm ntawm cov membrane-khi enzymes ntawm ion channels thiab receptor complexes, txhim kho lawv cov kev ua kom lig-khi, ua kom cov kev ua haujlwm ntawm neurotransmitters thiab lub xeev ntawm Lukyan. D. et al., 1993, A. K. Sariev li al., 2001). Lub xub ntiag ntawm mexidol nrog kev hloov pauv ntawm lub xeev ntawm synapses thiab channels qhia qhov tseem ua rau kev hloov kho tshuaj ntawm insulin cell receptors thiab muaj peev xwm potentiate cuam tshuam ntawm insulin.

2. Antihypoxic nyhuv ntawm derivatives ntawm 3-hydroxypyridine.

Lub luag haujlwm thoob ntiaj teb ntawm hypoxia hauv pathogenesis ntawm txhua txoj kev paub.

Qhov zoo tshaj yuav tseem muaj nyob rau hauv pathogenesis ntawm ntshav qab zib mellitus. Emoxipin muaj cov tshuaj tiv thaiv muaj zog thiab tsis txaus kev tiv thaiv kabmob (Lukyanova L.D. et al., 1993), Mexidol yog cov tshuaj tiv thaiv muaj zog (Lukyanchuk V.D. li al., 1998, Lukyanova L.D. et al., 1999). Qhov kev tiv thaiv ntawm Mexidol tshwm sim ntawm lub cev lub cev nyob rau hauv ntau yam ntawm hypoxia. Ntxiv mus, nws muaj peev xwm txo qis ATP nyob rau hauv cov ntaub so ntswg nyob rau hauv cov kev mob ntawm oxygen oxygen, nrog rau cov qub txheej txheem ntawm oxidative phosphorylation, i.e. Nws muaj cov nyhuv ncaj qha ua kom muaj zog (Devyatkina T.O. et al., 2000, Lukyanova L.D., 2002). Cov tshuaj tiv thaiv kev tiv thaiv ntawm emoxipin rau ischemia cuam tshuam tsis tsuas yog nrog nws lub zog tiv thaiv kab mob, tab sis theej nrog kev ua haujlwm ntawm kev hloov pauv, uas kom ua tiav ntau txoj haujlwm ntawm pawg ceev ceev ntawm tricarboxylic acid lub voj voog (Okovity S.V. li al., 2001). Cov lus tshaj tawm antihypoxic nyhuv ntawm Mexidol, raws li kev ua kom lub zog ntawm lub zog ntawm cov hlwb, tso cai rau peb xav txog nws ua kev yoo mov yoog raws li qhov tsis txaus ntseeg nyob rau hauv kev ntxhov siab, kev cuam tshuam rau cov teeb meem loj (Grechko A.T. li al., 1998, Smirnov L.D., 1998, Yasnetsov V.V. li al. ., 1999).

3. Qhov cuam tshuam ntawm derivatives ntawm 3-hydroxypyridine rau lipid muaj pes tsawg leeg ntshav cov ntshav thiab chav kawm ntawm IHD.

Raws li tau pom los ntawm kev sim thiab kev soj ntsuam, Mexidol qhia txog lub suab lipid-txo cov nyhuv zoo li hauv kev sim ntawm tus qauv ntawm kev tiv thaiv kev ntxhov siab (Inchina V.I. et al., 1996, 2000, Zorkina A.V., 1997, 1999.), ntawm tus qauv ntawm kev sim ntshav ntawm ntshav tsis ua hauj lwm hauv luav (Keleinikov S.B., li al., 2000). Kev sib xyaw ua ke ntawm hypolipidemic thiab antihypoxic kev tshwm sim qhia qhov kev ua haujlwm siab ntawm Mexidol hauv kev mob plawv ischemic mob plawv thiab myocardial infarction. Emoxipin pom muaj kev cuam tshuam cardioprotective hauv myocardial infarction zoo li hauv kev sim (Svetlikova I.V., 1994, Pashina I.V., 1995, Gatsura V.V. et al., 1996, Svetlikova I.V., Sernov L.N., 1996), thiab hauv chaw kho mob. Cov txiaj ntsig zoo ntawm cov teebmeem ntawm ob qho emoxipin thiab mexidol yog qhov tsis tuaj, hauv kev sib piv ntawm beta-blockers thiab calcium channel blockers, ntawm kev txiav txim siab cardiodepressant. Emoxipin txo cov ntu ntawm arrhythmias, qib ntawm lub plawv tsis ua haujlwm, thiab ua rau qeeb ntawm kev tsim cov necrosis hauv cov neeg mob uas muaj mob myocardial infarction (Lazebnik LB et al., 1994, Repin AN et al, 1994).Daim ntawv ntawm qhov ncauj mexidol mexicor ntawm ib koob ntawm 0.3 g ib hnub txo LPO, tag nrho cov roj cholesterol, LDL cov roj (cholesterol), apo-B thiab cov roj HDL ntau ntxiv hauv cov neeg mob uas muaj mob rau cov hlab ntshav (Mikhin V.P., 1998, 2002, Sernov L.N. et al. , Xyoo 1998, Guranova N.I., 1998), txhim kho kev ua haujlwm ntawm kev kho mob kom tsis muaj zog thiab txo cov ntshav tsis ua haujlwm ntawm sab laug ventricular myocardium (Pichugin V.V., Sernov L.N., 1998, Mikhin V.P. li al., 2002). Kev tswj hwm ntawm Mexidol hauv ib qho koob tshuaj ntawm mg / hnub rau lub lis piam nce cov kev ua ntawm endogenous AOS rau cov neeg mob laus (Mironov N.V. li al., 2002, Eremin P.A. li al., 2002, Katikova) O.V. et al., 2002).

4. Anticoagulant, antiplatelet thiab antithrombogenic cuam tshuam ntawm 3-hydroxypyridine derivatives.

Hauv kev siv ntawm kev tiv thaiv kev tiv thaiv ntawm 3-hydroxypyridine derivatives, lawv cov khoom antithrombogenic yog qhov tseem ceeb. Mexidol thiab lwm yam kev sib txuas ntawm 3-hydroxypyridine inhibit platelet kev sib cais, tiv thaiv cov ntshav liab los ntawm hemolysis, tiv thaiv kev hloov pauv ntawm cov nqaij mos ntawm thromboplastin, nce antithrombogenic muaj peev xwm ntawm lub vascular phab ntsa hauv kev sim atherosclerosis (Popov S.B., 1992, Spasov A.A. li al., 1997, 1999, 1999. Nazipova D.A. et al., 1999, Vintin N.A., 1999, Bruttseva N.A., 2000, Gavrilova L.V., 2001).

Kev sib xyaw ntawm cov teebmeem xws li hypolipidemic, antithrombogenic, antiaggregant, antihypoxic tuaj yeem yog lub hauv paus ntawm kev sim ntsuas txog qhov tshwm sim muaj txiaj ntsig ntawm cov tshuaj rau ntshav qab zib. Qhov lus xaus ntawm cov teebmeem no, suav nrog nootropic, kuj yog lub luag haujlwm rau lub siab lub hlwb cov haujlwm ntawm 3-hydroxypyridine derivatives (Mironov M.V. et al., 2001).

5. Qhov cuam tshuam los tiv thaiv thiab tshuaj tiv thaiv kab mob ntawm 3-hydroxypyridine derivatives yog vim muaj ntau cov txheej txheem: kev hloov kho ntawm kev sib koom tes ntawm macrophages thiab lymphocytes (Dorovskikh V.A. et al., 1999), nce ntxiv hauv cov ntsiab lus ntawm phosphoinositides nrog cov tshuaj tiv thaiv kev cuam tshuam hauv spleen hlwb (Bazanov G.A. et al., 1997, Demidova M.A., Popov D.A., 1999), kev hloov kho ntawm cytochemical thiab phagocytic kev ua ntawm granulocytes (Dubovskaya T.N., 1997).

Coj mus rau hauv lub luag haujlwm ntawm kev tiv thaiv kab mob pathology, suav nrog kev tsim ntawm autoantibodies rau pancreatic beta hlwb nyob rau hauv cov ntshav qab zib mellitus, cov tshuaj tiv thaiv immunomodulatory ntawm 3-hydroxypyridine derivatives tuaj yeem ua rau kev kho ntawm insulin tsis kam.

6. Hauv kev siv tshuaj tiv thaiv antitoxic nyhuv ntawm Mexidol, lub luag haujlwm tseem ceeb yog ua si los ntawm nws cov nyhuv hepatoprotein.

Hepatoprotective lub zog ntawm mexidol raug kuaj pom ntawm ntau yam qauv ntawm daim siab ua kom lub siab puas tsuaj. Thaum ntaus nrog tetrachloromethane, mexidol txo thaj tsam ntawm daim siab necrosis hauv luav (Keleinikova T.T., 1997). Nrog rau cawv, mexidol txo qhov degree ntawm kev puas tsuaj rau hepatocytes thiab nce cov ntsiab lus ntawm nucleic acids hauv lawv (Voronin T.A li al., 1997) .Txhua kev ua haujlwm los ntawm hepatotropic carcinogen dinitrosamine, cov tshuaj tiv thaiv ua rau muaj kev cuam tshuam nrog P-450, yog li ua rau muaj kev tiv thaiv zoo (Dumaev K.M. li al., 1995).

7. Cov txiaj ntsig ntsig txog kev tiv thaiv kab mob sib deev ntawm 3-hydroxypyridine.

Thaum lub sij hawm immobilization kev ntxhov siab, Mexidol poob qis ntawm epithelial dystrophy thiab edema ntawm cov tshuaj interstitial ntawm luav ob lub raum, txo qhov hnyav ntawm cov mob ntshav tsis txaus, muaj kev cuam tshuam cov hlab ntsha hauv lub raum, nce tus nqi ntawm glomerular filtration thiab secretory-excretory muaj nuj nqi ntawm lub raum

Shirshikova O.V., 1997). Cov tshuaj muaj nephroprotective zoo nyob rau hauv kev poob siab raug mob (Korolkova E.E., 2000). Hauv kev ua haujlwm ntawm Yu.I. Mashkov (2001), cov nyhuv nephroprotective ntawm Mexidol tau qhia tawm hauv kev sib xyaw ua ke aminoglycoside intoxication thiab mob hnyav nrog carbon tetrachloride. Tus sau qhia txog kev tiv thaiv cov tshuaj hauv alloxan mob ntshav qab zib hauv nas, thaum Mexidol, tsis zoo li dimephosphone thiab alpha-tocopherol, kho qhov nce ntawm qib ntawm triglycerides hauv lub raum.

Yog li, suav txog qhov tshwm sim ntawm 3-hydroxypyridine derivatives, muab ntau yam ntawm lawv cov teebmeem pharmacological, muaj peev xwm kho qhov yuav luag txhua qhov tseem ceeb ntawm cov kab mob ntshav qab zib mellitus yog LPO ua kom, tiv thaiv-tiv thaiv, cardio-tiv thaiv, hepato-, nephro-, angioprotective teebmeem, thiab kho cov hypercoagulemia. , tuaj yeem suav hais tias qhov ua tau zoo ntawm cov tshuaj rau ntshav qab zib. Thiab muab cov lus tshaj tawm hypolipidemic nyhuv ntawm cov tshuaj ntawm pab pawg no, nws cov kev tiv thaiv zoo li kuj muaj feem cuam tshuam nrog ntshav qab zib mellitus thiab exogenous hypercholesterolemia.

Ib txoj kev cia siab rau cov tshuaj kho ntawm cov teeb meem hauv cov ntshav hauv ntshav qab zib yog dimephosphon. Hauv kev ua haujlwm ntawm Khafizyanova R.Kh li al., (1993, 1994) nws tau qhia tias dimephosphon txhawb nqa ATP resynthesis thaum ischemia, txhawb kev ua haujlwm ntawm antioxidant enzymes. Cov tshuaj nce ntxiv • kev ua haujlwm ntawm qhov tseem ceeb enzyme glycolysis ntawm pentose phosphate shunt thiab tricarboxylic acid lub voj voog (Anichkova L.I. et al., 1992), ib txwm, ei CBS hauv acidosis, uas tshwm sim los ntawm kev mob raum thiab mob ntsws ntawm cov kua qaub-puag hauv lub xeev, nce ntshav ntawm cov ntshav thiab cov nqaij mos. metabolism hauv. Lipophilicity tso cai rau lub dimephosphon nkag mus rau lipid txheej ntawm daim nyias nyias ntawm lub xovtooj ntawm tes thiab ua rau pom cov kua-cov nyhuv-ua kom lub zog (Kinyabulatov A.I., 1996, Malyshev V.G., 1996). Cov ntaub ntawv sim tau tau ntawm cov tshuaj tiv thaiv kev ua haujlwm ntawm cov tshuaj nyob rau hauv lub siab ntev immobilization kev nyuaj siab (Zorkina A.V., 1994, 1997, Kudashkin S.S., 1996). Hauv kev siv ntawm kev tiv thaiv kev tiv thaiv dimephosphone nyob rau hauv kev sib xyaw ua ke los ntawm cov ntshav qab zib mellitus thiab hypercholesterolemia, nws cov nyhuv antioxidant, kev nce hauv cov kev ua ntawm glutathione peroxidase hauv lub plawv, lub hlwb, thiab lub siab yog qhov tseem ceeb (Geraskina MA, 1997). Kev tshawb nrhiav kev tshawb nrhiav qhia qhov kev cuam tshuam cardioprotective ntawm cov tshuaj. Dimephosphon thiab nws cov kev sib xyaw ua ke nrog dilzem thiab anaprilin ua pov thawj tawm tsam cov ischemic uas muaj lub cev ua haujlwm dhau thiab txo cov myocardial loj (N. Tyuryakhina, 2000). Ntau qhov kev cuam tshuam ntawm cov tshuaj pharmacological muab tau ib lub hauv paus rau kev kwv yees qhov ua tau zoo ntawm cov tshuaj hauv ntshav qab zib.

Yog li, kev soj ntsuam ntawm cov ntaub ntawv tshaj tawm qhia tau muaj qhov tshwm sim zoo ntawm cov tshuaj nrog cov tshuaj tiv thaiv antioxidant kev ua haujlwm ntawm cov ntshav qab zib mellitus sib cais thiab nws cov kev sib xyaw nrog exogenous hypercholesterolemia.

Tshooj Lus 2. Cov ntaub ntawv thiab cov hau kev tshawb nrhiav

Raws li cov hom phiaj thiab cov hom phiaj, cov txiaj ntsig ntawm mexidol hauv koob tshuaj thiab mg / kg, emoxipin hauv ib koob tshuaj 12,5 mg / kg, dimephosphone hauv koob tshuaj mg / kg thiab a - tocopherol hauv koob tshuaj mg / kg ntawm qee qhov ntsuas ntawm carbohydrate, lipid, protein tau kawm. metabolism, lub xeev ntawm lipid peroxidation system thiab antioxidant tiv thaiv nyob rau hauv cov ntshav ntshav thiab cov plab hnyuv siab raum hauv cov tsiaj ntawm kev sim nyob rau hauv kev sib txuas ua ke ntawm kev sim ntshav qab zib mellitus thiab exogenous hypercholesterolemia.

Ib qho kev tshawb nrhiav tau qhia rau cov kabmob dawb uas tsis muaj qwj ntawm cov pojniam ob leeg sib txawv hnyav ± 20 g. Cov tsiaj tau muab faib ua pawg:

I. Cov tsiaj txhu sib xws, uas thoob plaws qhov kev sim tau khaws cia ntawm cov zaub mov ntawm vivarium-10.

II. Cov tsiaj uas tau txhaj nrog cov roj oily tawm ntawm cov roj hauv cov hnub ntawm ib hnub ntawm mg rau ib kg ntawm tsiaj lub cev qhov hnyav, yav tas los yaj hauv 0.5 ml ntawm cov roj zaub. Txhawm rau txhim kho peroxide kev ntxhov siab, vitamin D tau ntxiv rau emulsion ntawm koob tshuaj ED ib kg ntawm huab hwm coj - 8.

III. Tsiaj tau txais rau ib os 0.5 ml ntawm cov roj zaub - 8.

IV. Tsiaj txhu nrog kev sim hyperglycemia - 12. Los tsim tus qauv ntawm kev sim ntshav qab zib mellitus, cov tsiaj yog ib zaug, tso tshuaj rau alloxan hauv koob tshuaj mg / kg. Txhawm rau ua kom tiav cov ntshav qab zib kom ruaj khov thiab ruaj khov, cov nas tau khaws cia ntawm cov zaub mov zoo rau hnub.

V.Pawg tswj xyuas muaj cov tsiaj nrog kev sim ntshav qab zib mellitus hauv kev sib xyaw nrog exogenous hypercholesterolemia - 10.

VI. Cov tsiaj nrog kev sim ntshav qab zib mellitus nyob rau hauv cov kev mob ntawm exogenous hypercholesterolemia, tib lub sijhawm cov roj cholesterol, tau txais txhua hnub subcutaneous mexidol ntawm ib koob tshuaj mg rau ib kg ntawm tsiaj lub cev qhov hnyav - 8.

VII. Cov tsiaj nrog kev sim hyperglycemia nyob rau hauv cov kev mob ntawm exogenous hypercholesterolemia tau txais txhua hnub subcutaneous mexidol ntawm ib koob ntawm mg rau ib lub cev qhov hnyav - 8.

Viii. Tsiaj txhu nrog kev sim ntshav qab zib hauv kev sib xyaw nrog hypercholesterolemia, tau txais emoxypine niaj hnub subcutaneously ntawm ib koob ntawm 12,5 mg rau ib kg ntawm tsiaj lub cev hnyav - 8 ib hnub.

IX. Cov tsiaj txhu nrog kev sib xyaw ntawm kev sim ntshav qab zib mellitus thiab hypercholesterolemia, uas tau muab dimephosphon ib hnub ntawm ib koob ntawm mg rau ib kg - 8 rau hnub.

X. Ib pab pawg ntawm cov tsiaj nrog kev sib xyaw ntawm kev sim ntshav qab zib mellitus thiab exogenous hypercholesterolemia, uas rau hnub, tau txais subcutaneous txhua hnub a - tocopherol ntawm ib koob ntawm mg / kg - 8.

Kev tuag ntawm cov nas uas muaj alloxan mob ntshav qab zib yog 25%. Ntawm pawg neeg tswj hwm, lub neej no yog 30%. Hauv qee pawg ntxiv, kev tuag ntawm tsiaj tsis tshwm sim. Cov tsiaj ntawm cov pab pawg II-IV raug tua nyob rau ntawm 15 hnub, V-X pawg nyob rau 29th hnub los ntawm decapitation nyob rau hauv ether tshuaj loog nrog lub sijhawm ua ntej 16-18 teev yoo mov. Ua ntej tua nyob rau hauv lub teeb ether maj pleev tshuaj loog, txhua tus tsiaj kaw ECG ntawm ib leeg-channel electrocardiograph siv rab koob hluav taws xob hauv peb tus qauv (I, II, III), peb qho tsis pub leej twg coj (aVR, aVL, aVF) thiab ib lub hauv siab (V4).

Thaum kawg ntawm kev sim, txhua tus tsiaj nyob rau hauv cov ntshav cov ntshav tau soj ntsuam cov zaub mov carbohydrate, lipid (tag nrho cov roj cholesterol, triglycerides, P - lipoproteins, lipoprotein cov roj ntshav siab ntau) thiab cov protein metabolism (tag nrho cov protein, albumin), transaminase kev ua si (ALT, ACT).

Qhov kev siv ntawm lipid peroxidation raug txiav txim los ntawm cov ntsiab lus hauv cov ntshav ntshav ntawm kev sim tsiaj ntawm cov khoom kawg ntawm lipid peroxidation - malondialdehyde (Konyukhova S.G., 1989). Lub xeev ntawm cov kab mob antioxidant tau txiav txim los ntawm cov kev ua hauv cov ntshav ntshav ntawm enzyme catalase (Korolyuk MA, 1988). Lub xeev ntawm lipid peroxidation thiab cov txheej txheem tiv thaiv antioxidant hauv cov tsiaj cov nqaij tau raug soj ntsuam los ntawm cov ntsiab lus ntawm malondialdehyde thiab catalase kev ua haujlwm hauv homogenates ntawm myocardium, mob siab, thiab lub raum.

Myocardial bioelectric kev ua ub no tau ntsuas los ntawm lub sijhawm ntawm PQ luv, qhov loj ntawm ntau yam ntawm QT luv, thiab tseem los ntawm qhov sib txawv ntawm QT luv, kho rau lub plawv dhia.

2.1. Cov ntaub ntawv kawm

Cov ntaub ntawv tshawb fawb yog ntshav thiab cov nqaij (myocardium, nplooj siab, raum) ntawm nas dawb. Ntshav tau coj los tom qab txiav tawm tag, khaws cia li ib teev ntawm chav sov thiab siv kom tau cov ntshav ntshav.

Txhawm rau kom ntshav ntshav, ntshav tau los nyob rau ntawm g rau feeb ntawm qhov TSRL-1 centrifuge.

Muab cov ntaub so ntswg homogenates.

Thaum kawg ntawm kev sim, cov tsiaj tau txi, lub plab ntawm lub plab tau qhib thiab lub siab thiab lub raum raug tshem tawm, tom qab ntawd lub hauv siab ntawm lub hauv siab tau qhib thiab lub siab raug tshem tawm. Lub raum yav tas los tau tso tawm los ntawm qhov tsiav tshuaj. Cov nplais ntawm cov nqaij mos tau txiav nrog txiab, huv si ntxuav los ntawm cov ntshav nrog chilled 0.9% sodium tshuaj dawb tov, qhuav nrog lim ntawv thiab muab tso rau hauv dej khov. Cov qauv ntawm cov ntaub so ntswg uas tau npaj rau qhov kev tshawb fawb tau muab tso rau hauv lub plooj (porcelain cug). Siv cov tshuaj tua tsiaj polished, meej homogenization tau ua nyob rau hauv kev xaiv hnyav rau kev sim (0.9% sodium chloride tov) hauv qhov sib piv ntawm 1: 9

2.2. Kev tshawb fawb txuj ci

Hauv cov ntshav cov ntshav, lipid metabolism tsis tau kawm txog: tag nrho cov roj cholesterol, triglycerides, cov roj lipoprotein ntau hauv cov roj lipoprotein siv cov khoom siv Olvex reagent cov khoom siv uas siv FP-901 biochemistry analyzer (Finland).Kev txiav txim siab txog qhov kev txiav txim siab ntawm (3 - lipoproteins tau ua tiav los ntawm enzymatic colorimetric method ntawm KFK-3 hluav taws xob photocalorimeter.

Cov kev ua haujlwm ntawm AlT thiab AcT cov enzymes tau txiav txim siab rau Hospitex Screen tus tswv ntxiv ntxiv rau kev ntsuas ib nrab tsis siv neeg (Switzerland) nrog txheej Hospitex kev kuaj mob.

Tag nrho cov protein tau tshuaj xyuas los ntawm cov tshuaj tiv thaiv biuret, cov feem ntawm cov protein tau txiav txim los ntawm electrophoresis ntawm lub tuam txhab Swiss "Hospitex" nrog lub computer densitameter.

Lus Txhais ntawm MDA (Konyukhova S.G., 1989).

Txhawm rau txiav txim siab plasma MDA, kev sib xyaw ua kom sib xyaw ua ke muaj 0.2 ml ntawm cov khoom siv ntsuas, 0.2 ml ntawm cov dej sib xyaw thiab 0.6 ml ntawm TBA hauv glacial acetic acid yog rhaub rau feeb, thiab tom qab txias, ntxiv 5 ml ntawm KOH thiab ml ntawm isopropyl cawv. Centrifuged ntawm 6000 rpm. tsis pub dhau min Hauv lub centrifugate, peb txiav txim siab qhov kev nqus kho qhov muag pom ntawm thiab nm tawm tsam kev tswj hwm uas muaj cov dej tsis hloov cov khoom siv sim. Qhov sib txawv hauv qhov ntom ntom ntuag tau txais kev pabcuam raws li kev ntsuas ntawm cov ntsiab lus ntawm MDA. Thaum txiav txim siab cov ntsiab lus ntawm MDA nyob rau hauv cov nqaij mos homogenates, lipid complex protein tau precipitated nrog trichloroacetic acid.

Kev ua haujlwm ntawm Catalase tau txiav txim siab hauv ntshav ntshav thiab cov nqaij mos homogenates ntawm kev sim tsiaj.

Kev txiav txim siab ntawm qhov kev ua ntawm catalase (Korolyuk MA, 1988).

Cov txheej txheem los txiav txim siab cov kev ua ntawm catalase yog raws li kev hloov pauv ntawm qhov ceev ntawm qhov muag pom tau los ntawm kev sib cuam tshuam ntawm hydrogen peroxide (022 02) nrog molybdenum ntsev.

Thaum txiav txim siab cov kev ua ntawm catalase, 0.13 ml ntawm H202 (ib qho qauv tsis muaj dej tsis muaj dej) ntxiv rau 0.1 ml ntawm cov kua roj ntsha. Tom qab feeb, cov tshuaj tiv thaiv raug tso tseg los ntawm kev ntxiv ml ntawm 4% ammonium molybdate. Qhov kev siv ntawm kev txhim kho xim tau ntsuas ntawm SF - ntawm lub teeb yoj ntawm nm tiv thaiv kev tswj H2 nrog rau kev ntxiv ml ntawm H2O - qhov kawg feem cuam tshuam.

2.3. Cov yam ntxwv ntawm pawg kho mob ntawm cov neeg mob

Hauv qhov chaw kho mob, qhov kev tiv thaiv zoo ntawm cov tshuaj kawm tau kawm hauv cov neeg mob uas muaj ntshav qab zib hom mellitus.

Cov neeg mob uas muaj hom 2 mob ntshav qab zib mellitus tau raug kuaj xyuas raws li endocrinology chav ua haujlwm ntawm Lub Tsev Haujlwm Hauv Nroog Thaj Chaw 4 ntawm Saransk. Cov neeg mob tau nyob rau theem ntawm cov ntshav qab zib decompensation thiab tau txais kev kho mob, nrog rau cov tshuaj tiv thaiv ntshav qab zib hauv lub cev, cov tshuaj metabolic, tshuaj uas txhim kho microcirculation, antihypertensive tshuaj. Txhua tus neeg mob tau ua qauv raws tus tub los ntxhais, hnub nyoog, qhov hnyav thiab lub sijhawm ua kom muaj tus kabmob, muaj cov kab mob concomitant pathology. Ntawm cov neeg kuaj mob 41% ntawm cov neeg mob txiv neej, 59% poj niam, 4.55% nyob rau pawg hnub nyoog txog rau xyoo, 45.45% rau cov hnub nyoog txog rau xyoo, 31.82% rau lub hnub nyoog txij li xyoo, 18.18% hauv lub hnub nyoog laus dua li xyoo. 22.73%) ntawm cov neeg mob uas muaj ntshav qab zib mus txog rau xyoo, 36.36%) ntawm cov neeg mob uas muaj mob ntev txog xyoo, 31-81%) muaj mob ntshav qab zib los ntawm xyoo txog xyoo thiab 9.09%) ntau xyoo. 45.45%) ntawm pawg neeg kawm muaj kev mob ntshav qab zib mellitus, 54.55% ntawm lawv tau muaj mob ntshav qab zib. Hauv txhua qhov tshuaj xyuas tus neeg mob, pom cov kabmob sib xyaw ua ke hauv daim ntawv ntawm IHD, mob ntshav qab zib, thiab lwm yam.

Txoj kev kawm tshawb no yog cov ntshav ntawm cov neeg mob. Cov ntshav rau kev kuaj mob tau coj los ntawm txoj hlab ntshav ntawm lub plab khoob.

Hauv kev ua haujlwm, qhov tshwm sim ntawm cov tshuaj ntawm lipid peroxidation cov txheej txheem (tshwm sim thiab tsim los ntawm cov hlau), lub xeev ntawm cov kab mob antioxidant hauv cov ntshav ntshav thiab erythrocytes, qib ntawm glycemia, kev ua haujlwm ntawm hemoglobin glycation thaum lawv tsim tawm hauv ib puag ncig uas muaj tag nrho cov ntshav ntawm cov neeg mob ntshav qab zib mellitus tau kawm.

Rau qhov no, tag nrho cov kev tshawb fawb tau muab faib ua series: koob thib 1 yog kev tswj hwm thiab suav nrog cov menyuam tsis tuaj yeem siv tshuaj, koob thib 2 tau muab tso nrog mexidol ntawm tus nqi ntawm 0.005 mg rau ib ml ntawm cov ntshav, koob thib 3 tau muab nrog mexidol ntawm koob tshuaj 0.025 mg / ml ntawm cov ntshav, koob thib 4 tau tsim nrog emoxipin ntawm koob tshuaj 0.0125 mg / ml ntawm cov ntshav, cov koob 5 tau tsim nrog dimephosphone ntawm tus nqi ntawm 0.050 mg / ml ntawm cov ntshav.

Cov pab pawg sib piv muaj kev noj qab haus huv (los ntawm cov kab no) cov tib neeg hnub nyoog tib yam.

Kev ntsuam xyuas ntawm kev siv ntawm lipid peroxidation tau ua tiav los ntawm kev sib txuam hauv cov ntshav ntshav thiab erythrocytes ntawm cov neeg mob ntshav qab zib mellitus ntawm cov lipoperoxidation theem nrab cov khoom lag luam - malondialdehyde thaum lub sij hawm tshwm sim thiab cov hlau ua rau lipid peroxidation raws li tus qauv ntawm S. Konyukhova li al. (1989). Txhawm rau txiav txim siab cov kev ua ntawm Fe-ntxias lipid peroxidation, ml ntawm 0.05 M daws ntawm hlau sulfate tau siv.

Lipid cia rau peroxidation hauv plasma thiab erythrocytes Kuv tau txiav txim siab los ntawm kev xam laij lej raws li tus qauv: Fe-MDA - MDA / MDA (Kuzmenko D.I., Laptev B.I., 1999).

Lub xeev ntawm cov kab mob antioxidant tau txiav txim los ntawm kev ua hauv cov ntshav thiab erythrocytes ntawm cov neeg mob ntawm lub zog tseem ceeb uas tiv thaiv hydrogen peroxide, catalase (Korolyuk MA, 1988).

Cov piam thaj hauv ntshav tau txiav txim siab los ntawm cov piam thaj oxidase txoj kev siv cov txheej txheem Photoglucose reagent (Moscow).

Lub zog ntawm hemoglobin glycation tau txiav txim siab los ntawm theem ntawm glycogemoglobin hauv qhov nruab nrab xeem. Nws cov ntsiab lus tau txiav txim siab siv tus qauv txheej txheem ntawm reagents Bio-LA-Test tuam txhab "Pliva-Lachema", (Czech koom pheej) ntawm kev tshuaj ntsuam biochemical. Lub hauv paus ntsiab lus ntawm cov qauv yog tias daim ntawv ruaj khov ntawm glycohemoglobin muaj 1-deoxy- (TM - valyl) fructose, uas yog lub cev qhuav dej nrog phosphoric acid los ua cov xim xim nrog cov adsorption ntau kawg ntawm nm. Tsis yog daim ntawv labile ntawm glycogemoglobin thiab tsis muaj menyuam hauv plab hemoglobin cuam tshuam nrog kev txiav txim siab.

Kev sib xyaw nrog qhov sib xyaw tau txheeb xyuas rau cov ntsiab lus ntawm cov kev kawm uas tau kawm nyob rau thawj feeb thiab tom qab ib hnub tsim tawm ntawm chav sov. Kev txiav txim siab ntawm cov piam thaj hauv cov ntshav cov ntshav dej tau ntxiv ntxiv ib teev tom qab pib tsim kom loj hlob.

Txhua qhov txiaj ntsig tau tau raug rau cov kev ua tiav ntawm lub computer ntiag tug uas siv cov Excel thov pob. Qhov tseem ceeb ntawm kev sib txawv raug soj ntsuam los ntawm Tub Ntxhais Kawm tsab ntawv t ntsuas.

Mexidol (3 - hydroxy - - methyl - - ethylpyridine succinate) - cov dej-soluble antioxidant - cov qauv tshuaj tivthaiv ntawm cov vitamins B6. Raws li cov qauv hauv tshuaj, mexidol yog ntsev ntawm succinic acid, succinate.

Pharmacological cov teebmeem ntawm Mexidol N

Nws tau tshaj tawm cov khoom siv antioxidant thiab membrane-tiv thaiv cov khoom, inhibits lipid peroxidation, sib cuam tshuam nrog lipid peroxides. Phenolic thiab hydroxyl radicals peptides thiab cov protein (Smirnov J1. D., 1995, 1998, 1999, Lukyanova L. D. et al., 1999).

Mexidol tsub kom cov kev ua si ntawm antioxidant enzymes lub luag haujlwm rau kev tsim thiab noj cov lipid peroxides, nrog rau hom kab mob oxygen oxygen. Nws tseem ua kom lub cev biological. Ua kom muaj kev sib txuas ntau ntawm cov polar lipid feem - phosphatidyl serine thiab phosphatidyl inosine, txo qis ntawm cov roj (cholesterol) / phospholipids, thiaj li txo qis viscosity ntawm lipid txheej (Smirnov L.D., 1995, Inchina V.I. et al., 1996, 2000, K. Dumayev, M.M. li et., 2002)

Cov mexidol pawg (3 - hydroxypyridine) khi rau cov roj ntsha raws roj ntsha, nkag rau hauv lawv, ua rau cov txheej txheem rov ua kom zoo dua qub thiab cuam tshuam cov kev nkag mus ntawm cov pa oxygen reactive rau cov roj fatty acid seem - cov teeb meem ntawm lipid peroxidation kev cuam tshuam. Mexidol tseem raug xa mus rau cyclic nucleotide phosphodiesterase inhibitors, nws nce cov ntsiab lus ntawm cAMP, qis platelet sib sau, thiab cuam tshuam rau lub zog metabolism.

Mexidol tuaj yeem ua raws li tus neeg saib xyuas tiv thaiv zoo nyob rau hauv kev ua ntawm ntau yam ua rau puas tsuaj thiab cov khoom pov thawj muaj zog ntxiv raws li daim nyias nyias, xov tooj cua, duab, hepatoprotector.

Nws ua ke ntawm kev cuam tshuam ntawm tranquilizers thiab cov tshuaj nootropic muaj cov nyhuv antihypoxic thiab tsis ua txhaum hemodynamics.

Cov teeb meem tshuaj ntawm dimephosphone

1,1 - Dimethyl - - oxobutylphosphonic acid dimethyl ether

Cov teeb meem pharmacological ntawm dimephosphone muaj ntau haiv neeg.Cov tshuaj ua rau lub ntsej muag hypothermic effect, antidote zoo thaum muaj kuab lom nrog cholinesterase inhibitors, cov nyhuv antacid, inhibits cov kev ua ntawm ntau tus enzymes, txhawb kev tsim tawm ntawm qee cov tshuaj hormones, thiab ua kom pom cov kev ua haujlwm neurotropic (Garaev RS, 1969, Gataulin I.A., 1980, Latfullin I.A. , 1985, Anichkova L.I. et al., 1991, Khafizyanova R.Kh., 1994).

Muaj ntau qhov tshwm sim ntawm cov tshuaj pharmacotherapeutic nyhuv ntawm dimephosphone tau tshawb pom thiab tshawb xyuas - tiv thaiv kev mob, mob kho kom zoo, ua kom lub cev puas tsuaj, tiv thaiv antihistamine thiab anti-serotonin (Svyatkina O.B., 1987, Blatun L.A. li al., 1991, Ziganshina L.E. et al., 1992).

Hauv ntau cov kev tshawb fawb, cov txheej txheem ntawm kev cuam tshuam ntawm dimephosphon rau kev ua ke ntawm cov platelets ntawm cov neeg tau txais kev noj qab haus huv, uas yog suav hais tias yog ua qauv ntawm cov txheej txheem ntawm kev ua haujlwm ntawm tes, tau kawm. Nws tau pom tias cov tshuaj inhibits platelet aggregation ntxias los ntawm ADP thiab adrenaline.

Cov kev coj ua ua ntej ntawm cov tshuaj pharmacological ntawm dimephosphone, uas txiav txim siab thaj chaw ntawm kev siv tshuaj kho mob, suav nrog nws cov kev cuam tshuam rau kev ua haujlwm ntawm intracellular Ca2 + ua tus tub xa xov theem nrab. Qhov kawg tshwm sim ntawm qhov kev ua ntawm dimephosphon yuav raug pom los ntawm kev tawm tsam kev ua haujlwm ntawm tes los ntawm kev cuam tshuam ntawm physiological antagonists - lub suab tshaj tawm los tiv thaiv H1 receptor nyhuv thiab qhov tsis meej xwm ntawm qib H2 receptor activation. Kev hloov kho tshuaj yog txuam nrog cov yam ntxwv ntawm kev sib cuam tshuam ntawm cov kab ke ntawm intracellular intermediaries.

Pharmacological cov teebmeem ntawm cov vitamin E

Ib qho tseem ceeb hauv lub luag hauj lwm ruaj khov ntawm cov txheej txheem dawb radical nyob rau hauv hlwb belongs rau cov vitamin E, uas muaj cov cuab yeej muaj zog tiv thaiv kab mob.

CH3 sn2- (CH2-CH2-CH-CH2) 2- (CH2) 2-CH sn.

Lo lus "vitamin E" yog hais txog kev zom cov roj nyeem ua kom muaj rog (tocopherols). Cov nquag siv ntawm cov no yog alpha-tocopherol. Alpha tocopherol yog nqus tau los ntawm cov kab mob lymphatic thiab thauj mus rau hauv kev sib txuas nrog chylomicrons. Hauv ntshav, alpha-tocopherol yog pom nyob hauv txhua feem lipoprotein, tab sis nws cov nyiaj ntau tshaj yog txuam nrog apo-B-lipoproteins. Hauv cov hlwb, nws cov ntsiab lus ntau tshaj plaws tau pom hauv mitochondria thiab hauv endoplasmic reticulum. Kev ua haujlwm tseem ceeb ntawm alpha-tocopherol yog kom ruaj khov ntawm cov yam ntxwv ua haujlwm thiab ua haujlwm ntawm cov roj ntsha. Alpha-tocopherol Acetate yog qhov tseem ceeb tshaj tawm cov roj-soluble antioxidant ntawm phenolic hom, nws ua lub luag haujlwm ntawm cov lipid peroxidation, muab kev tsim kom tsis muaj zog, tsis muaj peev xwm txhawb nqa cov saw kev hloov ntawm lipid peroxidation, radicals (Erin A.N. et al., 1998).

Cov hluav taws xob no ruaj khov heev, vim tias tsis muaj qhov ua kom tsis muaj hluav taws xob ntawm cov pa atom hauv C-6 txoj haujlwm tuaj yeem txav mus rau hauv cov qauv uas muaj lub nplhaib uas muaj ntxhiab, ua li ntawd ua rau lawv txoj kev nyob ruaj khov.

Tam sim no paub tias alpha-tocopherol tswj cov lipid txheej ntawm cov roj ntsha roj ntsha los ntawm tsawg kawg cov txheej txheem molecular, tiv thaiv: a) lipid peroxidation, b) cov kev puas tsuaj los ntawm singlet oxygen, c) phospholipid puas tsuaj los ntawm phospholipase A2, d) stabilizing lub cev lub cev (microviscosity) ntawm lipid bilayer. Ntxiv rau kev ua haujlwm ntawm "quenchers" ntawm cov dawb radicals thiab stabilizers ntawm cov cell week, vitamin E ua rau cov kab mob tiv thaiv kab mob ua kom muaj zog, nce kev ua haujlwm ntawm glutathione peroxidase (Vasilieva O.V. li al., 2000).

Tshooj 3. Cov txiaj ntsig ntawm mexidol, emoxipin, dimephosphone thiab α-tocopherol ntawm qee cov ntsuas kev ntsuas thiab ua haujlwm ntawm cov nas dawb nrog kev sib xyaw ntawm alloxan thiab exogenous hypercholesterolemia.

3.1. Cov nyhuv ntawm mexidol, emoxipin, dimephosphone thiab a - tocopherol ntawm cov metabolism hauv cov metabolism hauv cov nas dawb nrog kev sim ntshav qab zib mellitus tawm tsam keeb kwm ntawm hypercholesterolemia.

Kawm cov nyhuv ntawm kev sim alloxan mob ntshav qab zib nyob rau hauv tej yam kev mob ntawm hypercholesterolemia ntawm lub xeev ntawm cov khoom noj uas muaj cov metabolism hauv lub cev, kev hloov pauv ntawm cov kev tshawb fawb pom tseeb ntawm cov ntshav ntawm kev sim tsiaj tau qhia.

Kev tswj hwm rau cov nas alloxan hauv ib koob ntawm mg / kg pab txhawb kom muaj ntshav nce siab ntau ntxiv (ntawm 5.42 ± 0.10 mmol / L txog 9.85 ± 0.43 mmol / L, P 0.05 6.25 ± 0, 20 P 0.05 Pi 0.05 P2> 0.05 P2 0.05

Hauv% ntawm cov pib 135.20 87.50 124.79 192.71 121.21 110.43 114.09 119.51 114.42 cov ntaub ntawv

% Ntawm kev tswj 100.0 62.71 57.09 58.99 61.82 59.19

Roj HDL, 2.24 ± 1.80 + 2.48 ± 0.15 0.79 ± 0.04 0.59 ± 0.06 1.60 ± 0.05 1.85 ± 0.04 1.63 ± 0.03 1.46 ± 0.05 1.48 ± 0.07 mmol / L 0.08 0.05 P> 0.05 P 0.05 10.50 ± 0.67 P 0.05 Pi 0.05 Pi 0.05 8.67 ± 0.67 P 0.05 0.47 ± 0.02 P> 0.05 1.47 ± 0.02 P 0.05 0.65 ± 0.03 P emoxipine 12.5 mg / kg> mexidol mg / kg> a- tocopherol mg / kg ›dimephosphon mg / kg. Qib ntawm a - cov roj (cholesterol) tiv thaiv keeb kwm ntawm kev qhia txog Mexidol ntawm koob tshuaj mg / kg nce ntawm 0.59 ± 0.06 mmol / L txog 1,85 ± 0.04 mmol / L, i.e. ntau tshaj li lub sijhawm dhau qib tswj tau nce qib. Hauv emoxipin thiab mexidol mg / kg, qhov sib piv pharmacological zoo dua tau pom dua hauv qhov kev sim: theem ntawm HDL cov roj (cholesterol) hauv cov pawg tau nce mus rau 1.63 ± 0.03 mmol / L thiab 1.6 ± 0.05 mmol / L thiab dhau ntawm kev tswj hwm los ntawm 178 , 63% thiab 173.50%, ntu.

Cov lus qhia ntawm a - tocopherol thiab dimephosphone ua rau muaj qhov nce siab hauv qib theem ntawm cov roj lipoprotein ntau heev rau 1.48 ± 0.07 thiab 1.46 ± 0.05 mmol / L.

Yog li, qhia txog qhov hloov pauv ntawm qhov tau kawm txog kev ntsuas ntawm lipid metabolism, nws tuaj yeem sib cav tias cov nyhuv ntawm alloxan ntawm kev sim tsiaj ua rau muaj kev txhim kho ntawm cov ncauj lus lipid metabolism tsis zoo, nrog kev nce siab hauv cov theem ntawm (3-lipoproteins thiab triglycerides, los ntawm 80.0% thiab 193.60%, uas dhau los cov cim ntsuas tiv thaiv keeb kwm ntawm qhov txo qis hauv HDL cholesterol los ntawm 64.69% ntawm cov txiaj ntsig.Qhov kev hloov pauv no tau hais tias yog ntshav qab zib dyslipidemia.Qhov kev sib xyaw ntawm cov ntshav qab zib thiab cov cholesterol ua ke yog qhov tseem ceeb thiab tseem ceeb. Nws txawm exacerbated kev ntxhov siab uas tshwm sim, pab txhawb kev nce qib hauv qib ntawm atherogenic feem ntawm lipoproteins thiab triglycerides, uas tshaj qhov ntsuas ntawm cais alloxan ntshav qab zib los ntawm ntau tshaj ib yam.

3.3. Kev kho cov tshuaj ntawm tag nrho cov protein thiab albumin hauv cov nas dawb nrog kev sib xyaw ua ke rau alloxan thiab cov roj cholesterol.

Mob ntshav qab zib mellitus yog ib qho kab mob endocrine uas nrog cov kev ua txhaum ntawm txhua hom metabolism, nrog rau cov protein. Qhov no yog manifested mas nyob rau hauv lub weakening ntawm protein synthesis thiab ntau dua siv raws li lub zog siv. Kev ua txhaum ntawm cov synthesis thiab cov tawg ntawm cov protein ntau yog qhov pom tseeb ntawm kev ua kom lub zog ntawm proteolytic enzymes uas ua kom nws tawg (Lapteva NN, 1989), nrog rau qhov tshwm sim ntawm kev ua haujlwm ntawm lipid peroxidation, uas pib ua kev puas tsuaj rau cov qog ua qauv ntawm hepatocytes koom nrog nws cov synthesis (Matyushkin B.N. , Loginov A.S., 1996). Kev txwv tsis pub muaj protein ntau los ntawm cov amino acids yog qhov ua ntej rau kev tsim cov carbohydrates los ntawm lawv. Yog li, cov teeb meem hauv lub cev hauv lub cev ntshav qab zib mellitus yog qhov txawv txav ntawm cov protein synthesis thiab cov protein catabolism nrawm, uas ua rau muaj cov nitrogen tsis zoo.

Tawm tsam keeb kwm yav dhau los ntawm kev qhia txog alloxan, kev qhia txog lub cev ntawm cov khoom noj hauv lub cev thiab qhov ua rau lub siab ua tsis tau zoo hauv kev sim tsiaj ua rau lawv tus kheej muaj kev hloov pauv tseem ceeb hauv cov ntshav cov ntsiab lus ntawm kev sim cov tsiaj ntawm cov protein thiab albumin. Nyob rau 14 hnub tom qab tswj hwm ntawm alloxan, qhov tseem ceeb txo cov ntsiab lus ntawm ob qho tag nrho cov protein thiab albumin tau sau tseg (Cov Lus 3.3.1). Yog li, qhov kev txiav txim siab ntawm tag nrho cov protein cuam tshuam txo qis los ntawm theem ntawm cov tsiaj muaj zog ntawm 61.85 ± 1.85 g / l txog 42.46 ± 0.96 g / l, P 0.05 95.11 46.33 ± 0.67 P> 0 05 95.30

Zaub 60.58 ± 0.88 97.94 47.33 ± 1.33 97.36 roj P> 0.05 P> 0.05

Alloxan 42.46 ± 0.96 59.54 36.83 ± 1.17 75.76 mg / kg P 0.05). Kev qhia ntawm a-tocopherol ua rau muaj qhov nce siab hauv qib ntawm tag nrho cov protein rau 57.17 ± 1.83 g / l, uas yog 23.81% siab tshaj qhov tswj hwm tus nqi 46.17 ± 1.17 g / l thiab tsuas yog tsis ncav 7.59% lawm qib qhov tseem ceeb. Hais txog kev cuam tshuam rau tag nrho cov protein ntau, mexidol ntawm koob tshuaj mg / kg thiab a - tocopherol tau sib piv. Hauv cov ntawv no, nce ntxiv ntawm qib ntawm tag nrho cov protein tau sau tseg los ntawm 22.38% thiab 23.81%, feem. Dimephosphon yog qhov pom tau tias qis dua lwm cov tshuaj tau kawm txog qhov kev ua haujlwm tsis zoo, tab sis kev nce qib ntawm tag nrho cov protein kuj tseem ntseeg siab thiab tau npaum li 19.13% ntawm kev tswj qib.

Raws li qhov ua tau zoo ntawm cov tshuaj hais txog kev kho cov ntsiab lus albumin, cov tshuaj uas kawm tau tuaj yeem npaj raws li hauv qab no: Mexidol mg / kg> Mexidol mg / kg> Emoxipine 12,5 mg / kg.

Tawm tsam keeb kwm yav dhau los ntawm kev qhia mexidol ntawm koob tshuaj mg / kg, qib ntawm albumin ntau ntxiv los ntawm kev tswj tus nqi ntawm 32.96 ± 1.55 g / l txog 46.52 ± 0.87 g / l, tshaj nws los ntawm 41.11%, tab sis tsis tau ncav cuag si hauv cov tsiaj los ntawm 4.33%.

Pharmacological kev kho mob ntawm cov protein metabolism hauv cov nas dawb hauv cov kev sib xyaw ua ke ntawm alloxan thiab hypercholesterolemia M m m

Series Tag nrho cov protein, g / l Hauv% kom tshwm sim Hauv% tswj hwm Albumin, g / l Hauv% kom tshwm sim B% los tswj

Xav txog 61.85 ± 1.85 48.62 ± 1.72

Alloxan + roj cholesterol 46.17 ± 1.17 P 0.05 91.35 122.38 46.52 ± 0.87 P> 0.05 Pi 0.05 Pi 0.05 Pi 0.05 P2 0.05 P2 0 05 P, 0.05 92.41 123.81 30.40 ± 1.47 P 0.05 P2 0.05 P> 0.05

Alloxan 1.61 ± 0.05 + 97.55 1.45 ± 0.08 + 79.75

135 mg / kg P emoxipin. A-tocopherol thiab dimephosphone pom cov txiaj ntsig kev sib piv: qib ALT hauv cov koob no yog 1.10 ± 0.11 mmol / L thiab 1.10 ± 0.06 mmol / L, uas yog 37.54% thiab 37.37% los ntawm kev tswj kom haum. Qhov feem pua ​​ntawm txo nyob rau hauv AcT kev ua si nyob rau hauv cov pab pawg, suav tseem rau cov ntaub ntawv tswj, yog 26.94% thiab 22.70%, ntsig txog.

Hauv pawg ntawm cov tsiaj tau txais emoxipin, qhov kev poob qis ntawm Alt yog 57.17% thiab AcT los ntawm 20.84% ​​tau sau tseg hauv kev sib piv nrog kev tswj, i.e. cov nyhuv tsawg kawg pharmacological.

Cov nyhuv ntawm mexidol, dimephosphone, emoxipin thiab a - tocopherol ntawm cov kev ua ntawm transaminases hauv cov ntshav cov ntshav ntawm cov nas thaum raug alloxan thiab hypercholesterolemia M ± m

AlT series, mmol / L Hauv qhov tshwm sim Hauv% tswj AcT, mmol / L Hauv% kom tshwm sim B% los tswj

Khawb 0.82 ± 0.06 0.81 ± 0.06

Alloxan + roj cholesterol 2.93 + P 0.05 Pi 0.05 132.20 36.96 1.10 ± 0.07 P 0.05 135.94 71.71

Alloxan + roj cholesterol + mexidol 25 mg / kg 0.97 ± 0.06 P> 0.05 Pi 0.05 149.1 79.16

Alloxan + roj cholesterol + dimephos-xov tooj mg / kg 1,09 ± 0,06 Р 0,05 133,50 37,37 1,18 ± 0,04 Р 0,05 145,66 77,30

Alloxan + roj cholesterol + a-tocopherol mg / kg 1.10 ± 0.11 P 0.05 134.80 37.54 1.12 ± 0.08 P 0.05 138.42 73.06

Nco tseg: P - qhov tseem ceeb ntawm qhov sib txawv tau muab piv rau hauv kev sib raug zoo nrog theem, Pi - mus rau qib tswj (alloxan + roj), P2 - rau cov ntaub ntawv ntawm alloxan + roj cholesterol + mexidol pawg mg / kg

Daim duab 3.4.1 Qhov cuam tshuam ntawm qee yam antioxidants ntawm kev ua ntawm transaminases hauv cov ntshav ntshiab ntawm cov nas dawb nyob rau hauv kev sib txuas ua ke ntawm alloxan thiab exogenous hypercholesterolemia (hauv% ntawm kev tswj hwm)

1 - cov tsiaj zoo, - tswj theem (ntshav qab zib mellitus + hypercholesterolemia), - ntshav qab zib alloxan + hypercholesterolemia + mexidol mg / kg, - ntshav qab zib alloxan + hypercholesterolemia + mexidol mg / kg, - ntshav qab zib alloxan + hypercholesterolemia, / emgipin 12 kg - alloxan mob ntshav qab zib + hypercholesterolemia + dimephosphone mg / kg, - ntshav qab zib alloxan + hypercholesterolemia + a-tocopherol mg / kg, * - qhov tseem ceeb ntawm qhov sib txawv tau suav nrog hauv kev tswj cov ntaub ntawv

Yog li, nws tau ua raws los ntawm cov ntawv sau tseg yav dhau los hais tias kev tswj hwm alloxan mus rau kev sim tsiaj thiab cov txiaj ntsig ntawm cov roj cholesterol ua rau kev txhim kho cytolytic syndrome, raws li muaj pov thawj los ntawm qhov nce ntxiv hauv cov kev ua ntawm alanine thiab aspartic transaminases hauv cov pawg no. Kev sib xyaw ua ke ntawm cov yam tseem ceeb dua ua kom muaj kev puas siab ntsws citrlysis. Mexidol kho tau feem ntau kho los ntawm kev ua txhaum cai lij choj, ua rau muaj kev hloov kho ntawm ALT kev ua haujlwm rau cov nuj nqis uas nyob ze. Txawm li cas los xij, ACT kev ua haujlwm tseem nyob rau hauv cov ntshav ntshav txawm tias thaum kho, uas tej zaum qhia txog kev txhim kho ntawm qee qhov tsis tuaj yeem hloov pauv hauv lub cev ntawm kev sim cov tsiaj.

5.5. Cov nyhuv ntawm mexidol, emoxipin, dimephosphone thiab a - tocopherol ntawm qhov electrophysiological kev ua haujlwm ntawm myocardium hauv kev sim ntshav qab zib mellitus nyob rau hauv cov kev mob ntawm exogenous hypercholesterolemia.

Lub hauv paus tseem ceeb ua rau muaj kev xiam oob qhab loj thiab cov neeg tuag nyob hauv cov neeg mob ntshav qab zib yog cov kab mob plawv (myocardial infarction, lub plawv tsis ua haujlwm, mob stroke, peripheral angiopathies) (Shestakova MV, 2002). Lub luag haujlwm tseem ceeb hauv kev txhim kho vascular cov teeb meem ntshav qab zib mellitus belongs rau oxidative kev nyuaj siab thiab tsis-enzymatic autooxidative glycosylation (Balabolkin M.I. et al., 1999). Cov txheej txheem no ua rau puas tsuaj tsis tsuas rau cov hlab ntshav, tab sis kuj rau myocardium, txij li cov dawb radicals, oxidized cov protein muaj qhov ua rau lub cev puas tsuaj rau lub cev ntawm cardiomyocytes thiab cov hlwb ntawm cov hlab ntsws conduction system, txhawb kev apoptosis, pab cuam tshuam rau kev cuam tshuam ntawm cov dej num tsis zoo ntawm myocardium (Karpov Yu.A., Xyoo 2002). Yog li ntawd, kev kawm txog cov kev muaj peev xwm ntawm kev kho cov kev cuam tshuam myocardial kev cuam tshuam nrog kev pab ntawm antioxidants yog qhov muaj kev txaus siab heev.Hauv kev ua haujlwm no, peb tshawb xyuas cov txiaj ntsig mexidol, emoxipin, dimephosphone ntawm qee qhov electrophysiological ntsuas ntawm myocardium nyob rau hauv cov teebmeem sib xyaw ua ke ntawm kev sim ntshav qab zib thiab hypercholesterolemia.

Raws li cov txiaj ntsig ntawm peb qhov kev tshawb fawb (Cov Lus 3.5.1) qhia, kev tswj hwm cov roj (cholesterol) mus rau cov tsiaj sim ua rau muaj kev cuam tshuam ntawm lub plawv dhia (HR) los ntawm 397.06 ± 15.46 txog 513.0 ± 37.77 toj ib feeb, uas yog 29.20 % ntsuas kom dhau qib. Hauv cov pawg alloxan, tsis muaj qhov hloov pauv hauv lub plawv lub plawv tau tshwm sim. Kev sib xyaw ua ke ntawm kev sim ntshav qab zib mellitus thiab exogenous hypercholesterolemia cim kev nyiam ua kom lub plawv dhia mus rau 418.40 ± 16.10 ib feeb, txawm li cas los xij, cov txiaj ntsig no tsis muaj kev ntseeg tau. Sib piv cov txiaj ntsig tau hauv cov pawg kho mob nrog cov ntsuas ntsuas, peb tau txais tias: kev ntseeg siab kho lub plawv, rov qab mus rau qhov muaj nuj nqis, mexidol hauv koob tshuaj mg / kg (txo lub plawv los ntawm 418.40 ± 16.10 ib feeb hauv kev tswj kom 387.80 ± 14.84 ib feeb), emoxipin ntawm koob tshuaj 12,5 mg / kg (nce txog 376.95 ± 23.32 ib feeb) thiab a - tocopherol (nce txog 391.5 ± 27.7 ib feeb).

Hauv kev ua haujlwm, peb kuj tau txiav txim siab txog lub sijhawm ntawm PQ sib txuam ua ntej txhawm rau txhawm rau ntsuas lub xeev ntawm atrioventricular conduction. Nws tau pom tias kev tsim cov ntshav qab zib mellitus hauv kev sim tsiaj ua rau muaj kev nce siab hauv lub sijhawm ntawm PQ ntu ntawm 50.0 ± 2.86 ms txog 61.25 ± 2.19 ms, P 0.05 0.51 ± 0.03 P> 0, 05. 05

Alloxan mg / kg 381.36 ± 22.30 P> 0.05 61.25 ± 2.19 P 0.05

Alloxan + roj cholesterol 418.40 ± 16.10 P> 0.05 63.30 ± 3.18 P 0.05 P, 0.05 Pi> 0.05 P2> 0.05 8.57 ± 0.45 P> 0.05 P, 0.05 0.50 ± 0.02 P> 0.05 P, 0.05

Alloxan + roj cholesterol + mexidol 25mg / kg 427.78 ± 18.20 P 0.05 51.67 ± 2.78 P 0.05 P, 0.05 Pi 0.05 P,> 0.05 P2> 0.05 8.33 ± 0.56 P> 0.05 P, 0.05 0.52 ± 0.04 P> 0.05 Pi 0.05

Alloxan + roj cholesterol + dimephosphon mg / kg 405.97 ± 22.60 P> 0.05 P,> 0.05 P2 0.05 Pi> 0.05 P2> 0.05 8.75 ± 0.43 P> 0 .05 Pi 0.05 0.60 ± 0.05 P> 0.05 Pi 0.05

Alloxan + roj cholesterol + a - tocopherol ZOMg / kg 391.56 ± 27.70 P> 0.05 Pi 0.05 P2 0.05 0.67 ± 0.05 P> 0.05 Pi 0.05

Nco tseg: P - qhov tseem ceeb ntawm qhov sib txawv tau muab suav hais txog hauv qib, Pi - los tswj cov ntaub ntawv,

P2 - rau cov ntaub ntawv ntawm koob alloxan + roj cholesterol + mexidol mg / kg

Cov cawv ntawm mexidol, emoxipin, dimephosphone thiab a - tocopherol ntawm qhov hluav taws xob tsis khov ntawm myocardium nyob rau hauv cov kev sib xyaw ua ke ntawm alloxan ntshav qab zib thiab hypercholesterolemia (hauv% ntawm kev tswj hwm)

1 - sib luag, - alloxan + roj cholesterol, - alloxan + roj cholesterol + mexidol mg / kg, - alloxan + roj cholesterol + mexidol mg / kg, - alloxan + roj cholesterol + emoxipine 12.5 mg / kg, - alloxan + roj cholesterol + dimefosfon mg / kg kg, 7- alloxan + roj cholesterol + a- tocopherol mg / kg, * - qhov tseem ceeb ntawm qhov sib txawv tau muab suav rau hauv kev sib piv nrog qib tswj

Cov nyhuv ntawm cov kawm tshuaj tiv thaiv kab mob rau lub sijhawm PQ ntu nrog kev sib xyaw nrog kev sim ntshav qab zib mellitus thiab exogenous hypercholesterolemia (hauv% ntawm kev tswj hwm)

1 - sib luag, - tswj (alloxan + roj cholesterol), - alloxan + roj cholesterol + mexidol mg / kg, -alloxane + roj cholesterol + mexidol mg / kg, - alloxan + roj cholesterol + emoxipine 12.5 mg / kg, - alloxan + roj cholesterol + dimephosphon mg / kg, - alloxan + roj cholesterol + a-tocopherol mg / kg, * - qhov tseem ceeb ntawm qhov sib txawv yog xam nrog rau kev tswj qib

Yog li, cov txiaj ntsig ntawm peb txoj kev tshawb fawb qhia tau tias simulated pathology ua rau muaj kev cuam tshuam cov lus tsis txaus ntseeg nyob rau hauv kev ua haujlwm ntawm electrophysiological ntawm myocardium: tsis hnov ​​qab AV conduction, raws li qhia los ntawm kev ncua ntawm PQ luv (los ntawm 26,60%), hluav taws xob myocardial tsis txaus, lub hauv paus ntawm qhov uas yog qhov nce ntawm kev cuam tshuam ntawm QT cuam los ntawm 238 , 52%. Mexidol hauv ib koob ntawm mg / kg hloov kho txhim kho kom zoo ntawm kev siv hluav taws xob hauv lub atria (ua rau lub sijhawm PQ luv los ntawm 18.37% ntawm kev tswj hwm). Txhua yam ntawm kev kawm txog tshuaj tiv thaiv kab mob tiv thaiv kev txhim kho hluav taws xob myocardial kev tsis txaus ntseeg nrog kev sib xyaw ntawm kev sim ntshav qab zib mellitus thiab hypercholesterolemia, txo cov kev tawg ntawm QT luv los ntawm ntau dua 60%.

Tshooj 4. Cov txiaj ntsig ntawm mexidol, emoxipin, dimephosphone thiab atocopherol ntawm cov txheej txheem lipoperoxidation thiab cov haujlwm ntawm cov kab mob antioxidant hauv cov ntshav ntshav thiab cov nqaij ntawm cov nas dawb thaum kis alloxan tiv thaiv keeb kwm ntawm cov roj (cholesterol).

4.1. Cov nyhuv ntawm kev kawm txog antioxidant ntawm lipid peroxidation cov txheej txheem thiab cov haujlwm ntawm antioxidant enzymes hauv cov ntshav ntshav ntawm cov nas dawb nrog kev sib xyaw ntawm alloxan ntshav qab zib thiab hypercholesterolemia.

Ntau tus kws tshawb fawb pom tus txheej txheem ntawm cov tshuaj lom alloxan rau nws cov kev puas tsuaj los ntawm kev tsim cov dawb radicals (Baranov V.G., 1993, Yurina M.A., Adeykina O.A., 2000, Gard A., Grandy S., 1990). Raws li peb cov kev tshawb fawb tau qhia, kev tswj hwm ntawm alloxan mus rau kev sim tsiaj txhu txhawb kev nthuav dav tseem ceeb ntawm lipid peroxidation hauv cov ntshav ntshav. Peb tau txiav txim siab qhov hnyav ntawm lipid peroxidation los ntawm cov ntsiab lus hauv cov ntshav ntshav ntawm cov khoom LPO kawg - malondialdehyde. Nyob rau 14 hnub tom qab tswj hwm ntawm alloxan, kev nce MDA ntau hauv cov ntshav ntshav ntawm kev sim tsiaj tau sau los ntawm 5.8 ± 0.3 mmol / L txog 10.27 ± 0.3 mmol / L, P 0.05 + 22.0 23, 48 ± 1,02 p 0.05 -5.43 34.52 ± 0.81 p> 0.05 - 1.26

Alloxan mg / kg 10.27 ± 0.33 p 0.05 - 23.43 - 74.23 34.38 ± 1.29 P> 0.05 P, 0.05 -1.70 + 184.6

Alloxan + roj cholesterol + mexidol 25 mg / kg 4.13 ± 0.24 P 0.005 P, dimephosphon> a - tocopherol.

4.2. Cov nyhuv ntawm mexidol, emoxipin, dimephosphone thiab a - tocopherol ntawm lipid peroxidation thiab tiv thaiv antioxidant hauv cov nas myocardium nrog kev sib xyaw ntawm alloxan ntshav qab zib thiab exogenous hypercholesterolemia

Kev mob plawv ntshav qab zib yog qhov tseem ceeb tshaj plaws ua rau muaj kev tsis taus thiab kev tuag. Atherosclerosis nyob rau hauv cov neeg mob ntshav qab zib mellitus yog tus cwj pwm los ntawm kev txhim kho thaum ntxov thiab kev kis tus kab mob, uas tso cai rau peb los tham txog ntshav qab zib ua ib qho qauv ntawm atherosclerosis (Kozlov S.G., Lyakishev A.A., 1999, Haffner SM et al., 1990, Stamler J., et al., 1993). Nws paub tias lub luag haujlwm tseem ceeb hauv kev txhim kho vascular cov teeb meem ntshav qab zib yog los ntawm tsis muaj enzyme autooxidative glycosylation thiab oxidative kev nyuab siab (V. Lankin li al., 2000, V. Halliwell, 1999).

Yog li no, hauv txoj haujlwm no, peb tshawb xyuas lub xeev ntawm lipid peroxidation thiab tiv thaiv antioxidant hauv myocardium ntawm kev sim tsiaj nrog alloxan ntshav qab zib mellitus nyob rau hauv tej yam kev mob ntawm hypercholesterolemia.

Raws li cov txiaj ntsig ntawm peb cov kev tshawb fawb pom, qhov kev qhia ntawm alloxan tau pab txhawb kom muaj kev nce siab ntau hauv TBA, cov khoom siv tshuaj tiv thaiv, malondialdehyde hauv myocardium ntawm cov nas dawb, uas qhia tau tias ua kom muaj kev cuam tshuam tseem ceeb ntawm cov txheej txheem lipoperoxidation. Raws li hauv qab no los ntawm lub rooj 4.2.1, MDA qib tau nce siab los ntawm 5.78 ± 0.19 mmol / L hauv cov tsiaj ua si rau 18.84 ± 0.69 mmol / L hauv cov tsiaj ntawm cov ntawv kawm, uas tau nce mus txog 325.95% ntawm qhov tshwm sim thiab ntau tshaj li lub sij hawm tshaj qhov muaj nuj nqis ntawm qib lawm. Kev sib kis ntawm kev sim cov tsiaj rau cov roj (cholesterol) kuj ua rau muaj qhov nce ntxiv ntawm qhov kev nkag siab ntawm MDA nyob rau hauv myocardial homogenates mus rau 17.72 ± 0.58 mmol / L, uas nce siab tshaj qhov tsis sib luag los ntawm 206.77%.

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Qhov xaus ntawm kev hais tawm rau cov ncauj lus "Pharmacology, clinical pharmacology", Volkova, Natalya Anatolevna

Thov nco ntsoov tias cov ntawv pov thawj tshawb fawb tau hais los saum toj no yog rau kev siv nkaus xwb thiab tau txais los ntawm kev lees paub ntawm cov ntawv sau cov ntawv cuav (OCR). Hauv qhov txuas no, lawv yuav muaj qhov yuam kev cuam tshuam nrog qhov ua tsis tiav ntawm kev paub txog kev cim algorithms. Nyob rau hauv cov ntaub ntawv PDF ntawm kev hais tawm thiab cov ntawv sau tawm uas peb xa tawm, tsis muaj qhov yuam kev ntawd.

Cov ntawv tshawb fawb hluav taws xob hauv tshuab hluav taws xob disserCat - niaj hnub kev tshawb fawb ntawm Lavxias teb sab lus, cov lus, tshawb fawb tawm suab, cov ntaub ntawv tshawb fawb, cov ntawv sau ntawm kev tso tawm cov lus piav qhia.

Kev piav qhia thiab cov khoom

Emoxipin Nws yog cov hmoov uas muaj cov qauv siv lead ua thiab qib siab ntawm solubility hauv dej. Lub npe thoob ntiaj teb ntawm cov tshuaj nquag yog methylethylpyridinol.

Cov tshuaj muaj cov yam ntxwv ntawm cov tshuaj antioxidant thiab antihypoxant, nrog rau cov kab mob vasoconstrictor thiab antiplatelet tus neeg sawv cev. Lub zog antioxidant ntawm Emoxipin muab qhov nruab nrab ntawm cov dawb radicals, txiav tawm ntawm cov saw oxidative kev cuam tshuam, thiab, yog li ntawd, tiv thaiv kev puas tsuaj rau cov roj ntsha tseem ceeb hauv cov roj ntsha - DNA, cov protein, cov enzymes, cell membrane qauv, thiab lwm yam.

Cov cuab yeej ua haujlwm tiv thaiv ua rau Emoxipin tiv thaiv kom tsis txhob muaj pa oxygen ntawm cov plab hnyuv siab raum thiab cov ntaub so ntswg los ntawm kev xa cov roj ntau dua thiab txhim kho nws cov kev nkag mus los ntawm cov leeg ntsa thiab lub cell membrane.

Cov vasoprotective cov cuab yeej ntawm Emoxipin qhia hauv lub peev xwm los qhia lub zog, smoothness thiab elasticity rau lub nkoj ntsa. Ib txhij nrog qhov nce ntawm lub zog ntawm phab ntsa vascular, nws permeability txo.

Lub ntsej muag du ntawm cov hlab ntsha tso cai rau txo cov "ua ke ua ke" ntawm cov xov ntawm lub cev ntawm cov ntshav, nrog rau kev tiv thaiv lawv cov kev txhim kho ntawm cov phab ntsa ntawm cov leeg thiab cov hlab ntsha, uas ua kom muaj cov khoom tiv thaiv antiplatelet ntawm Emoxipin. Vim tias cov txiaj ntsig no, ntshav fluidity kuj txhim kho, uas yog, nws viscosity yog txo.

Ntxiv rau kev txo qhov "gluing" ntawm cov qe ntshav, Emoxipin txhim kho cov txheej txheem ntawm resorption ntawm cov ntshav txhaws, txo cov permeability ntawm cov hlab ntsha thiab tiv thaiv cov hemorrhages, thiab tseem txhawb lub nrawm resorption ntawm tom kawg. Hauv lub siab pathologies, Emoxipin siv qhov kev hloov kho vasodilating, txhawb kev thaj chaw hauv lub zos thiab txiav tawm lub qhov txhab tshwj xeeb thaum muaj mob plawv, ua kom lub zog ntawm kev mob plab thiab ua rau lub siab tsis zoo, tiv thaiv lub plawv tawg. Feem ntau, Emoxipin nce qhov kev tiv thaiv ntawm lub cev nqaij mus rau qhov tsis muaj oxygen thiab cov ntshav ncig.

Emoxipin daim ntawv thov

Cov txheej txheem kho mob siv cov khoom siv hluav taws xob nrog kev siv loj thiab ntau zaus xav tau kev tiv thaiv qhov muag los ntawm qhov tsis zoo ntawm cov txheej txheem no. Hauv cov xwm txheej no, Emoxipin yog siv los tiv thaiv lub qhov muag los ntawm ultraviolet thiab laser hluav taws xob, suav nrog tshav ntuj.

Cov neeg mob uas muaj qhov cuam tshuam txog ntawm choroid thiab ua haujlwm rau lub zog sib txawv ntawm cov kab mob, xws li lub ntsej muag txhawm siab, xav tau kev saib xyuas cov tshuaj Emoxipin tiv thaiv kev txhim kho kev puas tsuaj rau cov leeg thiab cov hlab ntsha ntawm lub cev ntawm lub zeem muag, thiab tswj lawv txoj haujlwm.

Ntxiv nrog rau kev xyaum ophthalmic, cov tshuaj no tau siv hauv kev kho plawv vim nws muaj kev tiv thaiv, nrog rau ntawm cov hlab ntshav ntawm lub plawv. Cov cuab yeej cardioprotective ntawm Emoxipin yog siv rau kev kho mob ntawm tus mob myocardial infarction, nrog rau kev tiv thaiv ntawm "reperfusion syndrome." Kev noj tshuaj Emoxipin txhim kho kev noj zaub mov zoo thiab metabolism hauv cov leeg nqaij tom qab lub plawv nres. Tsis zoo li lub siab tsis tuaj yeem tswj tau zoo dua nrog kev siv Emoxipin, thiab cov kev mob tshwm sim thiab kev tawm tsam ntau dua hauv lub siab ua rau tsis tshua hais tawm thiab tsawg tsawg.

Hauv kev xyaum mob neurological, Emoxipin yog siv los kho cov ntshav ncig ntawm lub hlwb ntawm ntau lub hauv paus pib. Ntxiv mus, cov tshuaj ua hauj lwm sib npaug zoo nyob rau hauv kev sib raug zoo rau sharply txo ntshav khiav thiab hemorrhage nyob rau hauv lub hlwb ntaub so ntswg. Tom qab kev phais mob txhawm rau tshem tawm cov hematomas uas nyob hauv thaj chaw me thiab hauv qhov chaw qis, cov tshuaj Emoksipin tso cai rau koj los ua kom cov ntshav ncig, thiab tiv thaiv kom tsis txhob mob ntshav tawm.

Niaj hnub no, Emoxipin yog siv los kho ib qho kev mob twg hauv cov txheej txheem ntawm cov kev tiv thaiv peroxidation, i.e. oxidative kev ntxhov siab, raug pom. Oxidative kev nyuaj siab yog pom nrog ntau yam kabmob, piv txwv li, nrog myocardial infarction, mob stroke, glaucoma, kis tus kab mob, thiab lwm yam.

Intramuscular thiab txhaj tshuaj rau tshuaj kho mob plawv thiab ntawm lub paj hlwb

2. Tsis pub dhau 10-30 hnub, 3% kev daws teeb meem ntawm Emoxipin yog muab tshuaj intramuscularly, 3-5 ml ib koob. Qhov qhia ntawm cov tshuaj yog nqa tawm 2-3 zaug hauv ib hnub.

Lub sijhawm sijhawm ntawm kev kho mob nrog Emoxipin ncaj qha yog nyob ntawm qhov sib txawv ntawm cov kab mob pathology, kev ceev nrawm ntawm kev rov ua haujlwm thiab qhov qub ntawm lub cev ua haujlwm.

Emoxipin Kev Txhaj Tshuaj rau Cov Tshuaj Kho Qhov Muag

Ophthalmologists siv txoj kev daws teeb meem 1% ntawm Emoxipin, thiab kev txhaj tshuaj yog ua nyob ze rau ntawm lub qhov muag (retrobulbar thiab parabulbar), zoo li nyob hauv qab conjunctiva (subconjunctival). Kev txhaj tshuaj ntawm Emoksipin parabulbarly nqa tawm ib hnub ib zaug lossis txhua lwm hnub, thiab txhaj nrog tshuaj tov 1% hauv ib qho li ntawm 0.5-1 ml. Hauv qab daim npog qhov ncauj, ib qho tshuaj 1% rau kev txhaj tshuaj yog tseem siv tau ib hnub, lossis txhua txhua lwm hnub, 0.2-0.5 ml. Subconjunctival thiab parabulbar tswj hwm ntawm Emoxipin yog nqa tawm hauv cov chav kawm ntev txog 10-30 hnub. Hauv ib xyoos hauv daim ntawv qhia hnub, koj tuaj yeem rov kho dua 2-3 zaug.

Nrog kev puas tsuaj rau lub qhov muag tob, txoj kev ntawm retrobulbar tswj hwm ntawm 1% kev daws teeb meem ntawm Emoxipin rau kev txhaj tshuaj yog siv. Cov chav kawm ntawm kev kho mob muaj ib zaug kev saib xyuas txhua hnub ntawm Emoxipin 1% hauv ib qho li ntawm 0.5-1 ml rau 10-15 hnub.

Txhawm rau tiv thaiv lub qhov muag thaum lub sijhawm laser coagulation manipulation, parabulbar lossis retrobulbar thawj coj ntawm 1% kev daws teeb meem ntawm Emoxipin hauv ib qho nyiaj ntawm 0.5-1 ml yog nqa tawm ob zaug - 24 teev thiab 1 teev ua ntej kev ua haujlwm. Tom qab phais mob rau 2-10 hnub, cov tshuaj tau muab rau hauv tib txoj kev, 0.5 ml ntawm 1% tov ib hnub ib zaug, txhua hnub.

Cov lus qhia tshwj xeeb rau kev siv Emoxipin

Yog tias tus neeg mob ntshav siab, tom qab ntawd siv Emoksipin yuav tsum ua nrog kev tshuaj xyuas ntshav siab tas li. Koj yuav tsum tau soj ntsuam cov ntshav txhaws tas li.

Yog tias Emoxipine ua rau cov tshuaj pleev qhov muag yuav tsum tau siv nrog lwm cov tshuaj hauv zos, tom qab ntawd yauv nws mus tom qab tsawg kawg li 10-15 feeb tom qab thov qhov kev kho dhau los.

Emoxipin yuav tsum tsis txhob xyaw nrog lwm cov tshuaj, tshwj xeeb tshaj yog kev sib koom tes ntawm cov tshuaj nrog lwm tus hauv cov koob txhaj tshuaj ib zaug tsis pub.

Qhov tshwm sim ntawm Emoxipin

Kev poob rau lub qhov muag tuaj yeem ua rau mob, mob, txhaws nrawm rau hauv lub qhov muag tom qab tswj hwm. Cov kev tsis zoo no feem ntau yuav ploj lawv tus kheej.

Kev txhaj tshuaj rau hauv Intraocular (retrobulbar, parabulbar, subconjunctival) ntawm Emoxipin tuaj yeem txuas nrog cov kev mob tshwm sim hauv qab no:

• mob ntawm chaw txhaj tshuaj
• khaus
• hlawv
• liab
• densification ntawm cov nqaij mos nyob ib ncig ntawm lub orbit ntawm lub qhov muag.

Kev tswj hwm ntawm Emoxipine hauv kev kho mob ntawm lub plawv thiab lub hlab hlwb tuaj yeem ua rau cov kev mob tshwm sim hauv qab no:

• txob taus rau lub sij hawm luv luv,
• tsaug zog
• nce me ntsis hauv siab
• kev ua xua hauv zos (ua pob ua pob, sawv pob, thiab lwm yam).

Emoxipin rau kev txhaj tshuaj thiab lub qhov muag - tshuaj xyuas

Emoxipin yog ib hom tshuaj uas ua tau zoo heev, tab sis nws muaj qhov ua rau thaj chaw tsis haum xeeb, uas ua rau tsis zoo siab thaum siv cov tshuaj hauv qhov muag. Cov neeg muaj kev txom nyem los ntawm cov kab mob qhov muag loj heev, thiab coj cov tee thiab txhaj tshuaj ntawm Emoxipin, suav txog qhov ntsuas thiab nkag siab meej txog qhov xav tau kev kho mob, tau txais txiaj ntsig zoo. Hauv qhov no, txoj kev xav zoo ntawm cov tshuaj feem ntau tau tsim thiab, raws li kev tshuaj xyuas kom zoo. Yog tias Emoxipin raug siv los kho cov mob me, thiab ib tus neeg tsis tau npaj siab yuav ua rau muaj qee qhov kev xav tsis zoo, tom qab ntawv qhov no los tshuaj xyuas qhov tsis zoo txog cov tshuaj, vim tias qhov xwm txheej no ua rau cov kev kho mob me me thiab cuam tshuam nrog kev tsis yooj yim.

Emoxipin rau kev txhaj tshuaj pab tshem tawm qhov tshwm sim ntawm kev mob plawv thiab mob nkees hauv ntau tus neeg mob uas muaj peev xwm txo tau qhov kev ua kom pom kev mob hlwb tsis zoo nyob rau lub sijhawm luv luv. Pab pawg neeg ntawm cov neeg mob no muaj kev paub zoo nrog kev siv tshuaj thiab, raws li, kev tshuaj xyuas kom zoo. Tsis tas li, cov neeg uas tau siv nws nrog lub hom phiaj ntawm kev txhim kho cov hlab hlwb khiav ceev thiab ceev resorption ntawm hematomas teb tau zoo txog cov tshuaj. Cov kev xav tsis zoo nrog kev siv tshuaj Emoxipine feem ntau yog tseg los ntawm cov neeg uas siv cov tshuaj ntawm lawv tus kheej los kho tus mob hu ua "ntshav tuab."