The role of oxygen-free radicals in ischemic tissue injury in island skin flaps.
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 hours 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 less than 0.005, and from 0/9 (0%) to 6/12 (50%), p less than 0.02, respectively. These findings are consistent with the hypothesis that oxygen free radicals generated at the time of reperfusion following a period of ischemia contribute significantly to the ultimate damage caused by ischemic 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.
D000818:Animals; D005260:Female; D005609:Free Radicals; D007511:Ischemia / Q000209:etiology / Q000473:pathology*; D009336:Necrosis; D010100:Oxygen; D010477:Perfusion / Q000009:adverse effects; D051381:Rats; D011919:Rats, Inbred Strains; D012867:Skin / Q000098:blood supply* / Q000187:drug effects; D013482:Superoxide Dismutase / Q000494:pharmacology; D013524:Surgical Flaps; D013997:Time Factors
D005609:Free Radicals; D013482:Superoxide Dismutase; D010100:Oxygen