Abstract
Summary In ischemic-reperfused myocardium severe cellular injury may develop rapidly upon re-oxygenation (‘oxygen paradox’). Several causes of this acute form of reperfusion injury have now been identified. During oxygen depletion cardiomyocytes accumulate Ca2+ in the cytosol. When re-energized upon re-oxygenation high cytosolic Ca2+ causes uncontrolled contractile activation, leading to hypercontracture of the myofibrils. Protection against hypercontracture can be achieved by various means, for example, by prolongation of ischemic intracellular acidosis or by attenuation of the oscillatory elevations of cytosolic Ca2+ in the early phase of re-oxygenation. Structural damage provoked by hypercontracture is favored by increased cytoskeletal fragility of the cardiomyocytes. In reperfused myocardium cardiomyocytes are also challenged by osmotic stress. Oxidative injury reduces sarcolemmal stability upon re-oxygenation and thereby reduces the tolerance of cardiomyocytes to osmotic stress. All these causes contributing to acute reperfusion injury are rooted within the myocardial cells. They are independent of exogenous, blood-borne factors that can additionally modify the reperfusion situation.
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