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

TLDR

The study investigated the contribution of free radical‑mediated reperfusion injury to ischemic damage from total venous occlusion of island skin flaps in a standardized rat model. The authors used this rat model of island skin flaps with total venous occlusion to assess reperfusion injury caused by free radicals. Control flaps with 8‑hour occlusion developed complete necrosis, whereas superoxide dismutase treatment before and after reperfusion significantly improved survival (from 0 % to 53 % and 50 % in two cohorts), supporting the hypothesis that oxygen free radicals at reperfusion cause ischemic injury and suggesting a therapeutic target.

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 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 < 0.005, and from 0/9 (0%) to 6/12 (50%), p < 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.