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Oxytocin protects rat heart against ischemia-reperfusion injury via pathway involving mitochondrial ATP-dependent potassium channel

Alizadeh, A.M. and Faghihi, M. and Sadeghipour, H.R. and Mohammadghasemi, F. and Imani, A. and Houshmand, F. and Khori, V. (2010) Oxytocin protects rat heart against ischemia-reperfusion injury via pathway involving mitochondrial ATP-dependent potassium channel. Peptides, 31 (7). pp. 1341-1345. ISSN 01969781 (ISSN)

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Abstract

Cardiac preconditioning represents the most potent and consistently reproducible method of rescuing heart tissue from undergoing irreversible ischemic damage. One of the major goals of the current cardiovascular research is to identify a reliable cardioprotective intervention that can salvage ischemic myocardium. The aim of the present study is to evaluate the oxytocin (OT)-induced cardioprotection and the signaling pathway involved with mitochondrial ATP-dependent potassium (mitoKATP) channel in the anesthetized rat heart. Animals were divided into six groups (n = 6): (1) IR; hearts were subjected to 25 min ischemia and 120 min reperfusion, (2) OT; oxytocin was administered (0.03 μg/kg i.p.) 25 min prior to ischemia, (3) ATO+OT; atosiban (ATO) was used as an OT-selective receptor antagonist (1.5 μg/kg i.p.) 10 min prior to OT administration, (4) ATO; atosiban was used 35 min prior to ischemia, (5) 5HD + OT; 5-hydroxydecanoic acid (5HD) was used as a specific inhibitor of mitoKATP channel (10 mg/kg i.v.) 10 min prior to OT administration, (6) 5HD; 5HD was used 35 min prior to ischemia. Then infarct size, ventricular arrhythmia and creatine kinase-MB isoenzyme (CK-MB) plasma level were measured. Hemodynamic parameters were recorded throughout the experiment. OT administration significantly decreased infarct size, CK-MB plasma level, severity and incidence of ventricular arrhythmia as compared to IR group. Administration of atosiban and 5HD abolished the cardiopreconditioning effect of OT. This study demonstrates that cardioprotective effects of OT are mediated through opening the mitoKATP channels. © 2010 Elsevier Inc. All rights reserved.

Item Type: Article
Additional Information: Unmapped bibliographic data: LA - English [Field not mapped to EPrints] J2 - Peptides [Field not mapped to EPrints] C2 - 20417240 [Field not mapped to EPrints] AD - Department of Physiology, School of Medicine, Tehran University of Medical Science, Enghelab Ave, Tehran, Iran [Field not mapped to EPrints] AD - Cancer Research Center, Tehran University of Medical Science, Tehran, Iran [Field not mapped to EPrints] AD - Anatomical Sciences Department, Faculty of Medicine, Gilan University of Medical Sciences, Rasht, Gilan, Iran [Field not mapped to EPrints] AD - Department of Pharmacology, Golestan Cardiovascular Research Center, Golestan University of Medical Sciences, Gorgan, Iran [Field not mapped to EPrints] DB - Scopus [Field not mapped to EPrints]
Uncontrolled Keywords: 5HD, Atosiban, Ischemia, Oxytocin, Reperfusion, 5 hydroxydecanoic acid, atosiban, creatine kinase MB, mitochodrial ATP dependent potassium channel, oxytocin, potassium channel, unclassified drug, animal experiment, animal model, animal tissue, article, controlled study, disease severity, drug efficacy, drug mechanism, enzyme blood level, heart hemodynamics, heart infarction prevention, heart infarction size, heart muscle ischemia, heart ventricle arrhythmia, male, nonhuman, priority journal, rat, reperfusion injury, signal transduction, Animals, Myocardial Reperfusion Injury, Oxytocin, Potassium Channels, Rats, Signal Transduction, Animalia, Rattus
Subjects: مقالات نمایه شده محققین دانشگاه در سایت ,Web of Science ,Scopus
موارد کلی
Divisions: معاونت تحقیقات و فناوری
Depositing User: GOUMS
Date Deposited: 20 Apr 2015 03:45
Last Modified: 05 Apr 2017 10:15
URI: http://eprints.goums.ac.ir/id/eprint/2200

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