Endogenous myocardial protection is the system of autodefense activated by the heart when undergoing ischaemic aggression. The best known mechanism is preconditioning, a phenomenon by which brief periods of reversible ischaemia improves myocardial tolerance to a later episode of prolonged ischaemia. It manifests itself by a reduction in infarct size, the improved contractile function which is sometimes observed being only a consequence. Although it was thought that the protection due to preconditioning was an early feature, that is to say occurring within 2 hours of the episode of initial preconditioning, it is now believed to confer protection up to 24 hours later. Early protection seems to depend on the activation of cell membrane receptors, especially those of adenosine which activate a chain of intracellular signals, the principal mediator being c-protein kinase, acting on ATP-dependant potassium channels. Late protection would seem to involve changes in expression of the cardiac genome leading to the synthesis of so-called stress proteins which have cardioprotective properties. The main value of studying these mechanisms of endogenous defense lies in the identification of their pharmacologic mediators, the use of which could open new perspectives in the treatment of ischaemic syndromes.