Ischaemia is a potent inducer of both myocyte necrosis and apoptosis in vitro. Thus, deprivation of oxygen alone, or in addition to serum withdrawal and deprivation of glucose, induces neonatal myocyte apoptosis. Ischaemia alone can induce apoptosis in the ischaemic territory in vivo, and this may be reduced by reperfusion. However, although reperfusion may limit ischaemia induced apop-tosis, reperfusion itself may accelerate the appearance of apoptosis in the reperfused regions.2
Myocardial infarction has been considered to be a prime example of necrotic cell death, because of the breakdown of cellular energy metabolism. However, apoptosis of cardiomyocytes also occurs in a temporally and spatially specific manner. Thus, acute myocardial infarction manifests both forms of cell death,3 with apoptosis particularly occurring at the hypoperfused "border" zones, between a central area of necrosis and viable myocardium. The central, unperfused region4 also manifests apoptosis, particularly within the first six hours, although between 6-24 hours necrosis is more common. Apoptosis in the remote non-infarcted myocardium may be partly responsible for myocardial remodelling and dilatation after myocardial infarction, and may be amenable to treatment.
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