مهار منافذ عبور میتوکندری باعث بهبود اثر محافظتی پس شرطی در قلب دیابتی می شود.

نجفی, مسلم and فرج نیا, صفر and محمدی نقده, مصطفی and بدل زاده, رضا and احمدی اصل, ناصر and برادران, بهزاد and امانی, محمد (1393) مهار منافذ عبور میتوکندری باعث بهبود اثر محافظتی پس شرطی در قلب دیابتی می شود. Journal of Diabetes & Metabolic Disorders ــ 13 (106). pp. 1-10. شاپا 2251-6581

Text - Published Version

Official URL: http://www.jdmdonline.com/content/13/1/106


Inhibition of mitochondrial permeability transition pore restores the cardioprotection by postconditioning in diabetic hearts

English Abstract

Background Cardiovascular risk factors, including diabetes mellitus may attenuate the cardioprotection by postconditioning. This study aimed to investigate the cardioprotective effect of ischemic-postconditioning (IPostC) against ischemia/reperfusion injury in normal and chronically type-1 diabetic rats and the effect of mitochondrial permeability transition pore (mPTP) inhibition in this field. Methods Diabetes was induced by a single intra-peritoneal injection of streptozotocin (50 mg/kg) in Wistar male rats (250-300 g). After 8 weeks, the hearts of control and diabetic animals were isolated and mounted on a constant-pressure Langendorff apparatus. All hearts were subjected to 30 min regional ischemia followed by 45 min reperfusion (by occluding and re-opening of LAD coronary artery, respectively). At the end of ischemia, the hearts received IPostC, cyclosporine-A, or both or none of them. Myocardial creatine-kinase (CK) release as an index of tissue injury was measured spectrophotometery in coronary effluent in reperfusion phase. Infarct size was identified by triphenyltetrazolium chloride staining. Heart rate, left ventricular end-diastolic pressure (LVEDP), LV systolic pressure (LVSP), rate-pressure product (RPP) and coronary flow were recorded throughout the experiment. Results IPostC, applied at the onset of reperfusion, failed to improve myocardial LVEDP and RPP, or reduce tissue damage indicated by infarct size and CK release in diabetic hearts, while it significantly recovered these parameters toward the pre-ischemic values in control hearts (P < 0.05). In contrast, with simultaneous inhibition of mPTP using cyclosporine-A, the cardioprotective effects of IPostC on myocardial hemodynamics, infarct size and CK release were significantly restored in diabetic hearts (P < 0.05). Conclusions The loss of cardioprotection by IPostC in diabetic state can be overcome by increasing the potency of protective IPostC through its co-application with mPTP inhibition.

Item Type:Article
زبان سند : انگلیسی
نویسنده :مسلم نجفی
نویسنده مسئول :صفر فرج نیا
نویسنده :مصطفی محمدی نقده
نویسنده مسئول :رضا بدل زاده
نویسنده :ناصر احمدی اصل
نویسنده :بهزاد برادران
نویسنده :محمد امانی
Additional Information:Indexing in: PubMed , PubMed Central , Scopus , Geobase Global Health , Index Copernicus , CABS , Cinahl , DOAJ , Embase , EmBiology , Fluidex
کلیدواژه ها (انگلیسی):Reperfusion injury; Diabetes; Postconditioning; mPTP; Cardioprotection
Subjects:QT physiology
WG Cardiovascular System
WK Endocrine System
Divisions:Faculty of Medicine > Department of Basic Sciences > Department of physiology
ID Code:6325
Deposited By: Dr Mohammad Amani
Deposited On:29 Oct 1393 06:04
Last Modified:10 Nov 1397 09:49

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