Postconditioning inhibits mitochondrial permeability transition

Evaluation of: Argaud L, Gateau-Roesch O, Raisky O et al.: Postconditioning inhibits mitochondrial permeability transition. Circulation 111, 194-197 (2005). The concept of preconditioning refers to the observation that short episodes of ischemia render the myocardium more resistant to damage due to subsequent prolonged ischemia and reperfusion. Recently, it was reported that a reduction of the myocardial infarct size could be obtained by brief intervals of ischemia applied not before, but immediately after, an episode of sustained ischemia; this phenomenon is known as postconditioning. The current experimental study conducted in rabbit hearts confirms that postconditioning can significantly reduce the extent of infarction. By demonstrating that mitochondria exposed to postconditioning display an increased resistance to ischemia/reperfusion injury and that postconditioning delays the calcium-induced opening of mitochondrial permeability transition pores, this study suggests that mitochondrial permeability transition is an important mediator of cardioprotection. The accumulation of experimental animal data suggesting that postconditioning could markedly limit irreversible myocardial injury caused by ischemia/reperfusion in humans leads to consideration of the applicability of such strategies in daily cardiology practice.