Limitation of infarct size by myocardial ischemic preconditioning
Myocardial ischemic preconditioning (IP) has caught the attention and imagination of researchers throughout the world (7). And for good reason: the magnitude of protection against ischemic injury conferred by IP is tremendous, far surpassing that offered by past pharmacological therapies. Although the original description of IP focused on limitation of myocardial infarction following acute coronary occlusion and reperfusion, IP may also decrease the incidence of ischemia-induced arrhythmias and improve post-ischemic cardiac function. However, in this article the discussion will be confined to the infarctlimiting effect of IP. Upon suffering a brief episode of ischemia, the myocardium instigates some change in itself which protects it from subsequent ischemic events. On an organ level the visible end-point is a decrease in infarct. This grossly visible change is the result of the cellular transduction of a signal and the institution of an adaptive cellular modification. But what precisely is that cellular process?
Key wordsIschemia-reperfusion myocardial infarction adenosine ATP-sensitive potassium channels protein kinase C
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