Reperfusion injury as a target for diminishing infarct size.

Therapies for preventing reperfusion injury (RI) have been widely studied. However, the attempts to transfer cardioprotective therapies for reducing RI from experiments into clinical practice have been so far unsuccessful. Pathophysiological mechanisms of RI are complicated and compose of many pathways e.g. hypercontracture-mediated sarcolemma rupture, mitochondrial permeability transition pore persistent opening, reactive oxygen species formation, inflammation and no-reflow phenomenon. Based on research, it cannot be determined which mechanism dominates, probably they cooperate with a domination of one or another in different clinical circumstances. Our hypothesis is, that only intervention that at the same time interferes with different (all?) pathways of RI may turn out to be effective in decreasing the final area of infarction.