Mechanisms of Cellular Alterations Due to Ischemia-Reperfusion Injury in the Heart

摘要: Reperfusion of the ischemic heart after a certain period time has been shown to produce cell injury. There is evidence show that alterations in mitochondrial metabolism during ischemia results accumulation H+ and this then leads activation Na+-H+ exchanger, Na+-Ca2+ exchanger development intracellular Ca2+-overload upon reperfusion. Changes massive release catecholamines their oxidation reperfusion oxyradicals other oxidants myocardium. This oxidative stress causes depression sarcolemmal Na+-K+ ATPase Ca2+-pump these changes also contribute towards occurrence Ca2+-overload. Both sarcoplasmic reticular Ca2+-cycling proteins as well myofibrillar defects result contractile dysfunction ischemic-reperfused hearts. Ischemic preconditioning some pharmacological interventions, which attenuate Ca2+-overload, have demonstrated reduce ischemia-reperfusion Thus it appears plays critical role induction myocardial damage due ischemia-reperfusion.