Infarct size-reducing effect of heat stress and α1 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. Therefore, we have investigated the implication of ai adrenoceptors in MS-induced resistance to myocardial infarction, in the isolated rat heart 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 antagonize alpha(1), alpha(1A) and alpha(1B) adrenoceptors. They were then either heat stressed (42 degrees C for 15 min) or sham anaesthetized. Twenty-four hours later, their hearts were isolated, retrogradely perfused, and subjected to a 30 min occlusion of the left coronary artery followed by 120 min of reperfusion. 3 Infarct-to-risk ratio was significantly 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% in HS+5MU vs 31.2+/-2.0% in Sham+5MU) and CEC-treated (33.4+/-3.0% in HS+CEC vs 32.4+/-1.3% in Sham+CEC) groups. Western blot analysis of myocardial HSP72 showed an MS-induced increase of this protein, which was not modified by Prat, 5MU and CEC pretreatments. 4 We conclude that both alpha(1A) and alpha(1B) adrenoceptor subtypes appear to play a role in the heat stressinduced cardioprotection, independently of the HSP72 level. Further investigations are required to elucidate the precise role of HSPs in this adaptative response.