Upregulated Hsp27 expression in the cardioprotection induced by acute stress and oxytocin in ischemic reperfused hearts of the rat.

In view of the cardioprotective effect of oxytocin (OT) released in response to stress, the aim of this study was to evaluate the role of heat shock proteins Hsps 70, 27 and 20 in stress-induced cardioprotection in isolated, perfused rat hearts. Rats were divided in two main groups: unstressed and stressed rats, and all of them were subjected to i.c.v. infusion of vehicle or drugs: unstressed rats [control: vehicle, OT (100 ng/5 μl), atosiban (ATO; 4.3 μg/5 μl) as OT antagonist, ATO+OT], and stressed rats [St: stress, OT+St, ATO+St]. After anesthesia, hearts were isolated and subjected to 30 min regional ischemia and 60 min subsequent reperfusion (IR). Acute stress protocol included swimming for 10 min before anesthesia. Malondialdehyde in coronary effluent was measured and the expression of Hsp 70, 27 and 20 was measured in myocardium using real-time reverse transcriptase polymerase chain reaction (RT-PCR). The malondialdehyde levels, which decreased in the St and OT groups, increased by the administration of atosiban as an OT antagonist. The expression of Hsp27 increased 4 to 5 folds by stress induction and i.c.v. infusion of OT. Central administration of atosiban prior to both stress and OT decreased Hsp27 mRNA levels. These findings suggest that endogenous OT may participate in stress-induced cardioprotection via Hsp27 over-expression as an early response.