Effects of Reperfusion on Infarct Size: Experimental Studies

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Abstract
Reperfusion of an ischaemic region in the dog heart has several possible consequences for the affected myocardium. The relative importance of each of these consequences depends on the severity and duration of blood flow deprivation, on whether the myocytes have been reversibly or irreversibly injured and on whether injury to the microvasculature has occurred. In this paper, the following important effects of reperfusion in ischemic myocardium are reviewed: (1) The acceleration of the disintegration of irreversibly injured myocytes by reperfusion results in contraction band necrosis. The sarcolemmal damage associated with this phenomenon permits accelerated washout of creatine kinase and other intracellular constituents. (2) Haemorrhage into the area of ischaemic injury results from reperfusion of tissue exhibiting severe ischaemic vascular injury. (3) Potentially fatal arrhythmias may be initiated by reperfusion. (4) Myocardial salvage occurs and infarct size is limited if reperfusion is instituted at a time when reversibly injured ischaemic myocytes at risk of necrosis are still present. In dogs there is a transmural ‘wavefront’ progression of irreversible ischaemic injury which occurs as a function of increasing duration of ischaemia; thus, the logical goal of very early reperfusion is complete prevention of celldeath and that of later reperfusion is the conversion of what might have been a transmural infarct to a nontransmural or subendocardial infarct. The time within which reperfusion can limit infarct size in experimental models of infarction is about 3 h. In some animals, small amounts of salvageable myocardium may persist beyond 3 h, but limitation of infarct size has not been demonstrated experimentally beyond 5–6 h. (5) Metabolic and functional recovery of surviving myocytes may require several days. Thus, the functional benefits of reperfusion may be underestimated if evaluated immediately after reperfusion.

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