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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

Nazari, A. and Sadr, S.S. and Faghihi, M. and Azizi, Y. and Hosseini, M.-J. and Mobarra, N. and Tavakoli, A. and Imani, A. (2015) Vasopressin attenuates ischemia-reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts. European Journal of Pharmacology, 760. pp. 96-102.

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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.

Item Type: Article
Additional Information: cited By 5
Uncontrolled Keywords: atractyloside; calcium chloride; creatine kinase MB; cyclosporin A; lactate dehydrogenase; malonaldehyde; vasopressin; antioxidant; carrier protein; mitochondrial permeability transition pore; vasopressin derivative, animal experiment; animal model; animal tissue; antioxidant activity; Article; controlled study; heart infarction size; heart mitochondrion; heart muscle ischemia; heart protection; lipid peroxidation; male; mitochondrial permeability; mitochondrion swelling; nonhuman; oxidative stress; priority journal; rat; reperfusion injury; animal; antagonists and inhibitors; drug effects; heart; metabolism; Myocardial Reperfusion Injury; physiology; Wistar rat, Animals; Antioxidants; Heart; Male; Mitochondria, Heart; Mitochondrial Membrane Transport Proteins; Myocardial Reperfusion Injury; Oxidative Stress; Rats; Rats, Wistar; Vasopressins
Subjects: مقالات نمایه شده محققین دانشگاه در سایت ,Web of Science ,Scopus
Divisions: معاونت تحقیقات و فناوری
Depositing User: GOUMS
Date Deposited: 08 Sep 2016 17:29
Last Modified: 17 Jan 2017 06:20
URI: http://eprints.goums.ac.ir/id/eprint/4673

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