The Role of Oxygen-free Radicals in Ischemic Tissue Injury in Island Skin Flaps

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Abstract
The contribution of free radical-mediated reperfusion injury to the ischemic damage caused by total venous occlusion of island skin flaps was investigated in a standardized rat model. Control flaps subjected to 8 h of total venous occlusion showed complete full thickness necrosis when followed for 7 days following release of the vascular occlusion. Treatment with superoxide dismutase, a scavenger of superoxide radicals, prior to and immediately following the onset of reperfusion, significantly enhanced island flap survival from 0/11 (0%) to 8/15 (53%), P < 0.005, and from 0/9 (0%) to 6/12 (50%), P < 0.02, respectively. These findings are consistent with the hypothesis that O2 free radicals generated at the time of reperfusion following a period of ischemia contribute significantly to the ultimate damage caused by ischemia injury. Such findings are consistent with similar reported observations on other tissues and suggest a means by which ischemic tissue injury might be therapeutically modified, even after the period of ischemia.