MYOCARDIAL PROTECTION DURING REPERFUSION

After prolonged periods of energy depletion, myocardial cells may rapi dly deteriorate during the early stage of reperfusion. It has now been clearly demonstrated that this kind of acute lethal reperfusion injur y is due to specific processes elicited by cellular re-energization. T he most prominent single cause of acute harm to the reoxygenated myoca rdial cells is myofibrillar hypercontraction. Hypercontraction is caus ed by a resupply of energy of the myofibrils at excessive cytosolic Ca 2+ concentrations. Additionally, the ability of the cytoskeleton to wi thstand large mechanical forces seems to be weakened after a prolonged period of energy depletion. Intracellular acidosis during the early s tage of reperfusion represents a natural mechanism of protection again st acute reperfusion injury, The reperfused myocardial cell may also s uffer from uncontrolled water uptake and increased sarcolemmal fragili ty, favoring osmotic damage of cell membranes. As yet therapeutical in terventions trying to specifically interfere with these pathomechanism s of reperfusion injury have only been tested experimentally, It seems promising to evaluate their utility for myocardial protection in card io-surgical operations.