Contribution of Upregulated HSPS Expression to The Cardioprotection Effect of Oxytocin Released in Acute Stress in Ischemic Reperfused Hearts of the Rat Download PDF

The heat shock proteins (HSPs) are expressed in normal cells but their expression is enhanced by a number of different stresses including heat and ischemia. The present study was aimed at determining the role of systemically released oxytocin in regulation of HSPs 70, 27 and 20 expression in stress- induced cardioprotection in isolated, perfused rat hearts. Rats were divided in to four groups: IR (Ischemia/Reperfusion), St (stress); rats exposed to swim stress for 10 min, St+ATO; atosiban was used as an oxytocin receptor antagonist (1.5mg/kg i.p.) prior to stress and ATO; atosiban was used prior to anesthesia. Hearts were isolated and subjected to 30 min regional ischemia and 60 min reperfusion (IR). Acute stress protocol consisted in swimming for 10 min. Ischemia-induced arrhythmias, Malondialdehyde in coronary effluent coronary flow, coronary flow and the expression of Hsp 70, 27 and 20 was measured in myocardium using real-time reverse transcriptase polymerase chain reaction (RT-PCR).The expression of Hsp 27 increased 4.5 folds by stress induction. Systemically administration of atosiban as an oxytocin antagonist prior to stress decreased Hsp27 mRNA levels. The malondialdehyde levels, which decreased in the St groups, increased by the administration of atosiban. These findings suggest that preconditioning effect of oxytocin at the periphery released in response to acute stress may be via Hsp27 over-expression as an early response.