INFARCT SIZE-REDUCING EFFECT OF HEAT-STRESS AND ALPHA(1) ADRENOCEPTORS IN RATS

1 Noradrenaline (NA), which is abundantly released during heat stress (HS), is known to induce both delayed cardioprotection and heat stress protein (HSP) 72 expression by the mediation of al adrenoceptors. The refore, we have investigated the implication of ai adrenoceptors in MS -induced resistance to myocardial infarction, in the isolated rat hear t model. 2 Rats were pretreated with prazosin (1 mg kg(-1), i.p., Praz ) or 5-methylurapidil (3 mg kg(-1), i.v, 5MU) or chloroethylclonidine (3 mg kg(-1), i.v., CEC) or vehicle Oil in order to selectively antago nize alpha(1), alpha(1A) and alpha(1B) adrenoceptors. They were then e ither heat stressed (42 degrees C for 15 min) or sham anaesthetized. T wenty-four hours later, their hearts were isolated, retrogradely perfu sed, and subjected to a 30 min occlusion of the left coronary artery f ollowed by 120 min of reperfusion. 3 Infarct-to-risk ratio was signifi cantly reduced in HS+V (15.4+/-1.8%) compared to Sham+V (35.7 +/- 1.3% ) hearts. This effect was abolished in Praz-treated (29.1 +/- 1.6% in HS + Prat vs 34.1 +/- 4.0% in Sham+Praz), 5MU-treated (34.5 +/- 2.2% i n HS+5MU vs 31.2+/-2.0% in Sham+5MU) and CEC-treated (33.4+/-3.0% in H S+CEC vs 32.4+/-1.3% in Sham+CEC) groups. Western blot analysis of myo cardial HSP72 showed an MS-induced increase of this protein, which was not modified by Prat, 5MU and CEC pretreatments. 4 We conclude that b oth alpha(1A) and alpha(1B) adrenoceptor subtypes appear to play a rol e in the heat stressinduced cardioprotection, independently of the HSP 72 level. Further investigations are required to elucidate the precise role of HSPs in this adaptative response.