%0 Journal Article
%T Preconditioning effects of oxytocin in reducing cardiac arrhythmias in a rat heart regional ischemia-reperfusion model
%A Mahdih Faghihi
%A Ali Mohammad Alizadeh
%A Vahid Khori
%A Vahid Khodayari
%J Physiology and Pharmacology
%D 2013
%I Iranian Society for Physiology and Pharmacology
%X Introduction: Occurrence of cardiac arrhythmias and myocardial infarction are two main deleterious events that are caused by ischemia-reperfusion (IR) injury in the heart. Cardiac preconditioning represents the most potent method of rescuing heart tissue from undergoing irreversible ischemic damage. The aim of the present study was to evaluate oxytocin (OT) cardioprotective effects and its signaling pathways in cardiac arrhythmias including ventricular tachycardia (VT) and ventricular fibrillation (VF) in anesthetized rats. Methods: Fifty-four rats were divided into nine groups. Animals¡¯ hearts were subjected to 25 min ischemia and 2 h reperfusion. Oxytocin was used 25 min prior to ischemia. In certain groups, atosiban (an oxytocin receptor antagonist), atractyloside (an opener of mitochondrial permeability transition pore, mPTP) and N-acetylcysteine (a reactive oxygen species scavenger) were used 10 min prior to OT administration. Then, the severity and incidence of cardiac arrhythmias including VT and VF were measured. Results: OT administration significantly decreased the severity and incidence of cardiac arrhythmias compared to the IR group (P<0.05). Administration of atosiban, atractyloside and N-acetylcysteine abolished the cardiac preconditioning effect of OT in cardiac arrhythmia (P<0.05). Conclusion: The present study demonstrates that preconditioning with oxytocin reduced ischemia-reperfusioninduced ventricular arrhythmias and its signaling pathways are probably mediated through mitochondrial permeability transition pore and reactive oxygen species.
%K Ischemia-reperfusion
%K oxytocin
%K cardiac arrhythmia
%K atractyloside
%K N-acetylcysteine.
%U http://www.phypha.ir/ppj/browse.php?a_code=A-10-624-2&slc_lang=en&sid=1