Influence of Anti-Inflammatory Drugs and Free Radical Scavengers on Intestinal Ischemia Induced Oxidative Tissue Damage

Abstract

The model of intestinal ischemia, effected by an occlusion of the superior mesenteric artery, seems to be well suited to assess the contribution of oxygen free radicals in this ischemic disease and, by using different free radical scavengers, the sources of these oxidative metabolites as well. Thus, because there is substantial body of evidence that neutrophils are one of the major sources of free radicals, a treatment of intestinal ischemia by antibiotics can be helpful (Lutz and Augustin, 1989). These antibiotics manage a diminution of chemoattractants for neutrophils, leading to an only slight activation of these cells. There is still a controverse discussion about the tissue damaging activity of myeloperoxidase in vivo by generation of the oxidant HOC1. Many clinical data indicate only a slight toxicity, which is in contradiction to the high reactivity of OC1^- (for review see Weiss, 1989). In spite of that, other findings show an oxidative damage done by hypohalous acids if myeloperoxidase can first bind to its target. This damage is believed to be a hypochlorous acid damage because of the high concentration of C1^- compared to other halides in body fluids.