Document Detail


Oxytocin protects rat heart against ischemia-reperfusion injury via pathway involving mitochondrial ATP-dependent potassium channel.
MedLine Citation:
PMID:  20417240     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 microg/kg i.p.) 25 min prior to ischemia, (3) ATO+OT; atosiban (ATO) was used as an OT-selective receptor antagonist (1.5 microg/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 (10mg/kg i.v.) 10 min prior to OT administration, (6) 5HD; 5HD was used 35min 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.
Authors:
Ali Mohammad Alizadeh; Mahdieh Faghihi; Hamid Reza Sadeghipour; Fahimeh Mohammadghasemi; Alireza Imani; Fariba Houshmand; Vahid Khori
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-22
Journal Detail:
Title:  Peptides     Volume:  31     ISSN:  1873-5169     ISO Abbreviation:  Peptides     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-05-31     Completed Date:  2010-09-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8008690     Medline TA:  Peptides     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1341-5     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
Affiliation:
Department of Physiology, School of Medicine, Tehran University of Medical Science, Enghelab Ave, Enghelab Squ, Tehran, Islamic Republic of Iran.
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MeSH Terms
Descriptor/Qualifier:
Animals
Myocardial Reperfusion Injury / prevention & control*
Oxytocin / pharmacology*
Potassium Channels / metabolism*
Rats
Signal Transduction*
Chemical
Reg. No./Substance:
0/Potassium Channels; 0/mitochondrial K(ATP) channel; 50-56-6/Oxytocin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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