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

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 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.

journal_name

Peptides

journal_title

Peptides

authors

Alizadeh AM,Faghihi M,Sadeghipour HR,Mohammadghasemi F,Imani A,Houshmand F,Khori V

doi

10.1016/j.peptides.2010.04.012

subject

Has Abstract

pub_date

2010-07-01 00:00:00

pages

1341-5

issue

7

eissn

0196-9781

issn

1873-5169

pii

S0196-9781(10)00166-X

journal_volume

31

pub_type

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