Reperfusion therapy is the primary treatment for acute myocardial infarction. Its infarct-limiting effectiveness is, however, limited by so called reperfusion-induced myocardial injury likely related to reperfusion-mediated opening of the mitochondrial permeability transition pore (mPTP). While pharmacologic cardioprotection has proved to effectively reduce infarct size in the experimental models its clinical usefulness is problematic. In this context, a clinical exploitation of endogenous cardioprotective mechanisms, known as ischaemic preconditioning and ischaemic postconditioning, emerges as an attractive therapeutic alternative. This is particularly so because ischaemic pre- and post-conditionig seem to afford cardioprotection by preventing reperfusion-induced deleterious opening of mPTP.
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