Abstract
Postischemic intestinal tissue damage is induced at least partly by the enhanced formation of oxygen radicals. The initial source of oxygen radicals is the hypoxanthine-xanthine oxidase system. Oxygen radicals react directly with polyunsaturated fatty acids leading to lipid peroxidation within the cell membranes. Indirectly, these radicals trigger the accumulation of neutrophils within the intestinal tissue initiating inflammatory processes which lead to severe mucosal lesions. Various substances (superoxide dismutase, catalase, dimethylsulfoxide, allopurinol, and deferoxamine, etc.) are able to detoxify oxygen radicals or inhibit the mechanisms leading to enhanced generation, thus attenuating the postischemic lesions of the mucosa. Collectively, the data from an increasing body of literature imply that oxygen radicals are instrumental in the development of hemorrhagic mucosal lesions after intestinal ischemia. These lesions can be prevented even when the treatment starts during ischemia and before reperfusion.
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