Pathophysiology and mediators of ischemia-reperfusion injury with special reference to cardiac surgery. A review.

Abstract

Although necessary for the ultimate tissue survival, reperfusion may paradoxically exacerbate the ischemic injury. Ischemia and reperfusion injury is intimately woven together. The relative role of reperfusion injury is not clarified and probably varies with the ischemic insult: Reperfusion is always preceded by ischemia, and some of the reperfusion-related events may represent a process continuing from the ischemic period; thus the proper designation should be ischemia-reperfusion injury. The reperfusion-related events are: arrhythmias, myocardial stunning with both systolic and diastolic dysfunction, and low reflow and microvascular stunning. Of pathogenetic importance are the mode and speed of reperfusion as well as the initiation of an intracoronary inflammatory reaction during reperfusion, including endothelium-leukocyte interaction, platelets, generation of oxygen free radical, generation and release of arachidonic acid metabolites, platelet activating factor, endothelium derived relaxing factor, endothelins, kinins, and histamine, complement activation, disturbances in calcium homeostasis, and disturbances in lipid and fatty acid metabolism.