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As other preconditioning phenomena, heat stress is able to induce a delayed myocardial protection against ischaemia-reperfusion injury by preserving ventricular function, preventing arrhythmia occurrence and reducing cellular necrosis. The development of heat stress response has been extensively studied in order to characterize the different steps of this form of preconditioning. It appears that chemical signals (such as nitric oxide, reactive oxygen species (ROS)) released by sublethal hyperthermic stress trigger a complex cascade of signalling events that include activation of protein kinase C (PKC) and mitogen-activated protein kinases (MAPK) and culminate in increased synthesis of inducible nitric oxide synthase, cyclooxygenase-2, antioxidant enzymes and protective proteins such as heat stress proteins (Hsps). A better understanding of this powerful protective adaptation of the cardiomyocyte is essential for the development of clinical applications and the design of cardioprotective pharmacological agents. The purpose of this letter is to review current information regarding the characteristics of heat stress preconditioning compared to other forms of late preconditioning.

Heat stress (HS) is known to induce delayed protection against myocardial infarction. We have previously shown that inducible nitric oxide synthase (iNOS), was involved in mediating this form of preconditioning. Since iNOS and cyclooxygenase-2 (COX-2) are co-induced in various cell types, the goal of this study was to investigate whether COX-2 could also participate to the HS-induced cardioprotection.A total of 78 male Wistar rats, subjected to either heat stress (42 degrees C for 15 min) or sham anaesthesia were used for this study. Twenty-four hours later, they were treated or not with a selective COX-2 inhibitor, either celecoxib (3 mg kg(-1), i.p.) or NS-398 (5 mg kg(-1), i.p.), 30 min before being subjected to a 30-min occlusion of the left coronary artery followed by a 120-min reperfusion, in vivo. HS resulted in a marked increase in myocardial COX-2 protein expression at 24 h, associated with a significant protection against infarction (46.0+/-1.4% in sham vs. 26.8+/-3.8% in HS group) (Por=0.05). Administration of selective COX-2 inhibitor 24 h after HS, completely abrogated this delayed cardioprotection (46.4+/-3.6 and 48.0+/-2.8%, respectively, in HS+celecoxib and HS+NS-398 groups).This study provides the first evidence of an implication of COX-2 as a mediator of HS-induced cardioprotection. This suggests that prostaglandins are involved in this type of cardioprotective preconditioning.