Colonic healing: a role for polymorphonuclear leucocytes and oxygen radical production

Abstract

Using a model of 'reperfusion injury' as a mechanism of oxygen radical (OR) production in vivo, we have demonstrated that superoxide (O2-) is the major source of damage. Inhibition of its production from polymorphonuclear leucocytes (PMNs) by aprotinin, a protease inhibitor, or by scavenging with superoxide dismutase (SOD), resulted in reduced oxidation of of tissue glutathione (P less than 0.002). Colonic healing after anastomosis was also improved by aprotinin as measured by histology (P less than 0.05), breaking energy (P less than 0.001), breaking strength (P = 0.02), and by hydroxyproline content (P = 0.01). Allopurinol, although inhibiting glutathione oxidation, had no effect on PMN leucocyte OR production and did not protect against histological damage. These data demonstrate that PMNs endogenous to the tissue or attracted there as a result of trauma are the source of OR production in 'reperfusion'. Their inhibition improves colonic healing.