title: Vasopressin attenuates ischemia-reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts.
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.
authors.affiliation: Department of Physiology, School of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran.
authors.forename: Afshin
authors.initials: A
authors.lastname: Nazari
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Electrophysiology Research Center, Neuroscience institute, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Seyed Shahabeddin
authors.initials: SS
authors.lastname: Sadr
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Mahdieh
authors.initials: M
authors.lastname: Faghihi
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Yaser
authors.initials: Y
authors.lastname: Azizi
authors.affiliation: Zanjan applied Pharmacology Research Center, Zanjan University of Medical Sciences, Zanjan, Iran.
authors.forename: Mir-Jamal
authors.initials: MJ
authors.lastname: Hosseini
authors.affiliation: Department of Biochemistry and Biophysics, Metabolic Disorders Research Center, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran.
authors.forename: Naser
authors.initials: N
authors.lastname: Mobarra
authors.affiliation: Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Asadollah
authors.initials: A
authors.lastname: Tavakoli
authors.affiliation: Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: aimani@tums.ac.ir.
authors.forename: AliReza
authors.initials: A
authors.lastname: Imani
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D014667:Vasopressins / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D014667:Vasopressins
keywords: Free radical; Heart; Ischemia/reperfusion; Mitochondrial swelling; Vasopressin