The reperfusion of acute ischaemic myocardium is essential for myocardial salvage, so-called "gold standard" therapy, however it can result in serious damage to the myocardium. Functional alterations occur, including depressed contractile function and decreased coronary flow as well as altered vascular reactivity. Over several decades it has been demonstrated that oxygen radical formation is greatly increased in the post-ischaemic heart and serves as a critical central mechanism of ischaemic-reperfusion injury. However it has been demonstrated that free radicals play an important role in the endogenous adaptation phenomenon of the heart, too. Ischaemic preconditioning is a cellular adaptive response of the heart to stress, which provides the most potent endogenous protection against reperfusion arrhytmias, stunning and infarction. Post-conditioning defined as brief periods of ischaemia and reperfusion during the very early minutes of reperfusion stimulates endogenous adaptation. Post-conditioning may also attenuate the damage to endothelial cells and cardiomyocytes from oxidants, cytokines, proteases and inflammatory cells.
Keywords: endogenous adaptation; endogén adaptáció; free radicals; myocardial ischaemia-reperfusion; szabad gyökök; szívizom ischaemia-reperfúzió.