Early reperfusion phenomena.

Cycles of ischemia-reperfusion are ubiquitous in clinical cardiology. Depending on the duration and intensity of the ischemic episode as well as its repetition mode, several pathophysiologic syndromes have been identified, such as myocardial stunning, hibernation, and preconditioning. It remains a difficult exercise to distinguish ischemic from reperfusion damage. Production of oxygen free radicals and alteration in calcium homeostasis are major players during early reperfusion, responsible for the pathologic and functional alterations. At the molecular level, upregulation and downregulation of a number of genes have been observed in stunned myocardium, pointing toward some inborn survival adaptive mechanism. The no-reflow phenomenon, a most paradoxic event after reperfusion, usually occurs after more prolonged episodes of ischemia. The underlying mechanism involves additional lesions to the microvasculature interacting with myocytes lesions. Further insight into molecular and genomic adaptation to ischemia and reperfusion will undoubtedly help to improve our ability to fight reperfusion injury.