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Vasopressin Attenuates Ischemia-Reperfusion Injury Via Reduction of Oxidative Stress and Inhibition of Mitochondrial Permeability Transition Pore Opening in Rat Hearts Publisher Pubmed



Nazari A1 ; Sadr SS2, 3 ; Faghihi M2 ; Azizi Y2 ; Hosseini MJ4 ; Mobarra N5 ; Tavakoli A6 ; Imani A2
Authors
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Authors Affiliations
  1. 1. Department of Physiology, School of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran
  2. 2. Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Zanjan Applied Pharmacology Research Center, Zanjan University of Medical Sciences, Zanjan, Iran
  5. 5. Department of Biochemistry and Biophysics, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
  6. 6. Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

Source: European Journal of Pharmacology Published:2015


Abstract

Aim of this study was to investigate the involvement of the mitochondrial permeability transition pore (MPTP) and oxidative stress in the cardioprotective effect of vasopressin (AVP) on ischemia/reperfusion (I/R) injury. Anesthetized male wistar rats were subjected to regional 30 min ischemia and 120 min reperfusion and randomly divided into nine groups: (1) Control; saline was administered intravenously before ischemia, (2) vasopressin was administrated 10 min prior to ischemia, (3, 4) Atractyloside as MPTP opener, was injected 5 min prior to reperfusion without and with vasopressin, (5, 6) Cyclosporine A as a MPTP closer, was injected 5 min prior to reperfusion without and with vasopressin, (7) mitochondria were isolated from control group and CaCl2 was added as MPTP opener and swelling inducer, (8) isolated mitochondria from Control hearts was incubated with Cyclosporine A before adding the CaCl2 (9) CaCl2 was added to isolated mitochondria from vasopressin group. Infusion of vasopressin decreased infarct size (18.6±1.7% vs. control group 37.6±2.4%), biochemical parameters [LDH (Lactate Dehydrogenase), CK-MB (Creatine Kinase-MB) and MDA (Malondialdehyde) plasma levels, PAB (Prooxidant-antioxidant balance)] compared to control group. Atactyloside suppressed the cardioprotective effect of vasopressin (32.5±1.9% vs. 18.6±1.7%) but administration of the Cyclosporine A without and with vasopressin significantly reduced infarct size to 17.7±4% (P<0.001) and 22.7±3% (P<0.01) respectively, vs. 37.6±2.4% in control group. Also, vasopressin, similar to Cyclosporine A, led to decrease in CaCl2-induced swelling. It seems that vasopressin through antioxidant effect and MPTP inhibition has created a cardioprotection against ischemia/reperfusion injuries. © 2015 Elsevier B.V. All rights reserved.
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