| Background and aimsThe most effective method of limiting acute myocardial ischemic necrosis is reperfusion; however, the effects of reperfusion itself may be associated with polymorphonuclear leukocyte (PMN) accumulation, a burst of oxygen free radical production, activation of inflammation, intracellular calcium overload, which may result in paradoxical cardiomyocyte dysfunction, a phenomenon termed " reperfusion injury".Evidence of cadiofnyocyte apoptosis has been extensively documented after reperfusion of an acute ischemia. Apoptosis of cardiomyocte was not only seen in cultured cell in vitro, but also universally in animal ischemia reperfusion model and autopsied myocardial samples of human that died of acute myocardial infarction. Apoptosis is the main form of cell death in the early stage of myocardial reperfusion. Apoptotic cardiomyocytes were particularly in the border zones of infracted myocardium, whereas very fews cells were present in the remote noninfarcted myocardium. A subset of myocytes undergo apoptosis during ischemia reperfusion and post myocardial infarction, which enlarges the infracted size of myocardium and increases cardiac mobidity and mortality. Necrosis and apoptosis are distinct mechanisms of cell death. Apoptosis induced by ischemia reperfusion associated with activation or de novo expression of proteins and genes. Bcl-2/Bax and Fas genes in which regulates apoptosis, and its expressed products play a very important central roles.The precise mechanisms of ischemia reperfusion injury remain unclear. There is still no effect methods to attenuated or protect ischemia reperfusion injury. The research of efforts to protect myocardium in the current era of reperfusion by thrombolysis or percutaneous coronary intervention has focused on limitation of irreversible reperfusion injury. Preconditioning (PC) is presently considered the most effect endogenous protect...
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