[Oxygen radicals and postischemic organ damage--pathophysiology, clinical relevance and therapy]

Abstract

Postischemic damages after ischemia and reperfusion are of growing clinical relevance. It was assumed that these damages were due to hypoxia. It has been shown that during reperfusion oxygen radicals are generated in high concentrations adding significantly to the damage. These oxygen radicals are generated by the hypoxanthine-xanthine oxidase system. They do not only damage directly but trigger the accumulation and migration of PMN-leukocytes within the inflicted tissue. PMN-leukocytes induce a non-specific postischemic inflammatory reaction which is responsible for the severe reperfusion damages. Oxygen radicals can be treated successfully by so-called radical scavengers. Thereby, it is essential to initiate the therapy during the so-called "therapeutic window", a time interval in which reperfusion aggravates the ischemic lesions. Only few clinical studies have been performed. The results concerning scavenger treatment after myocardial infarction have been disappointing. In transplantation surgery, however, antioxidative therapy has proven to be beneficial. Well-defined double blind randomized well-stratified clinical studies are now essential in order to assess the possibilities of antioxidative therapy after time-limited ischemia and reperfusion.