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Cardiovascular Research 2003 60(3):469-477; doi:10.1016/j.cardiores.2003.08.012
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Heat stress preconditioning and delayed myocardial protection: what is new?

Marie Joyeux-Faure*, Claire Arnaud, Diane Godin-Ribuot and Christophe Ribuot

Laboratoire HP2, Hypoxie Physio-Pathologies Respiratoire et Cardiovasculaire, Faculté de Pharmacie de Grenoble, Domaine de la Merci, 38706 La Tronche, France

*Corresponding author. Tel.: +33-476-637-475; fax: +33-476-637-108. Email address: marie.faure{at}ujf-grenoble.fr

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.

KEYWORDS Heat stress; Preconditioning; Myocardial ischaemia

Time for primary review 21 days


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