The role of allopurinol in preventing oxygen free radical injury to skeletal muscle and endothelial cells after ischemia-reperfusion.

One of the most important mechanisms in the production of ischemic damage after replantation surgery is the rise of oxygen free radicals during revascularization of ischemic tissues. Free radicals produce damage in the cell membranes (lipoperoxydation). This occurs not only in muscle tissue, but also in endothelial cells, with a consequent increase of local edema and the risk of compartment syndrome. This study attempted to interrupt the ischemic-reperfusion injury process in ischemic rat hindlimbs. Complete ischemia was induced for different numbers of hours (3, 6, 9, 12 hr) in four groups of rats (24 animals in each group). Allopurinol, an oxygen free radical scavenger, was tested in solution, 12.5 mg/kg b.w., in half the studied animals (n = 12). Collected data showed an increase (mean value: 0.60 nM/mg 3 hri 0.90 nM/mg at 6 hr; 0.80 nM/mg at 9 hr; 0.89 nM/mg at 12 hr; mean value in nonischemic muscle = 0.526 nM/mg) in lipoperoxides (NS between treated/untreated groups, p > 0.05) and high tissue pressure values in the posterior compartment of the ischemic rat hindlimbs. Allopurinol reduced the pressure values (p < 0.05 in Groups 1-3; p < 0.1 in Group 4), but was not effective in reducing lipoperoxides in skeletal muscle.