Abstract

Brief myocardial ischemia/reperfusion has complex effects on the myocardium. In the short term the myocardium may be stunned with temporarily reduced contractile function, though this may also be accompanied by the modification and de novo synthesis of proteins that protect the heart against subsequent early or delayed insults. Repeated episodes of non-lethal ischemia, which are common in the clinical setting, combine all of these phenomena and may ultimately result in chronic contractile dysfunction. Nitric oxide is intimately linked to many of these alterations in cellular function and defense. This article examines data predominantly from in vivo large animal studies that relate to these ischemia-induced changes, the evidence for the proposed mechanisms behind both myocardial stunning and preconditioning while concentrating on the role of nitric oxide in these conditions.

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