ABSTRACT
Experimental evidence available currently indicates that injury to the muscle during reperfusion is most likely mediated by oxygen-derived free radicals (oxyradicals). The major oxyradical generating system in the skeletal muscle has yet to be identified so that an appropriate oxyradical-generating inhibitor and/or scavenger can be selected for the prevention of ischemia-induced reperfusion injury to the skeletal muscle. In addition, apart from generating oxyradicals, the activated leukocytes, platelets, and vascular endothelial cells are also known to synthesize and release vasoconstrictive substances and/or chemoattractants for leukocytes. The role of these locally released chemical substances in the pathogenesis of ischemia-induced reperfusion injury in muscle flaps has yet to be elucidated. The pathophysiology of ischemia-induced reperfusion injury to the skeletal muscle in muscle flaps is reviewed.
