Role of leukocytes and tissue-derived oxidants in short-term skeletal muscle ischemia-reperfusion injury

The relative contribution of xanthine oxidase (XO) and leukocytes to tissue injury after short-term ischemia is unknown. In this study, we subjected t hree groups of rat spinotrapezius muscles to 30-min ischemia and 1-h reperf usion: 1) ischemia-reperfusion (I/R) + 0.9% saline, 2) I/R + superoxide dis mutase, and 3) I/R + oxypurinol. A fourth group served as nonischemic contr ol. We quantified the increase in resistance (%Delta R) caused by leukocyte -capillary plugging concurrently with myocyte uptake of propidium iodide (P I) [expressed as no. of PI spots per total volume of perfused tissue (N-PI/ V)] and performed assays to quantify XO activity, thiobarbituric acid-react ive substances (TBARS), and myeloperoxidase (MPO). Groups 2 and 3 exhibited significant decreases in N-PI/V relative to group 1. MO levels and TEARS w ere similar among all groups, and mean %Delta R was significantly reduced i n groups 2 and 3 relative to group 1. However, elevated XO was observed in groups 1 and 2 relative to group 3 and nonischemic controls. These data are consistent with the hypothesis that XO, rather than toxic species produced by plugging or venule-adherent leukocytes, is responsible for postischemic damage in this model.