Infarct size-reducing effect of heat stress and α₁ adrenoceptors in rats

Abstract

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 α₁ adrenoceptors. Therefore, we have investigated the implication of α₁ adrenoceptors in HS-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 (V) in order to selectively antagonize α₁, α_1A and α_1B adrenoceptors. They were then either heat stressed (42°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+Praz 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 HS-induced increase of this protein, which was not modified by Praz, 5MU and CEC pretreatments.

4. We conclude that both α_1A and α_1B adrenoceptor subtypes appear to play a role in the heat stress-induced cardioprotection, independently of the HSP72 level. Further investigations are required to elucidate the precise role of HSPs in this adaptative response.

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