[The bowel as an ischemic organ].

Due to the progress that has been made in intensive care, more and more patients survive shock. It is a clinical observation that their condition improves substantially with the restoration of intestinal function. Different experimental models have been developed to investigate the pathophysiology of the intestine in shock. As noxious periods, both the phase of ischemia and the phase of reperfusion have been identified. Since the experimental models are methodologically very different, the results of the various studies may only be compared with reservations. Nevertheless, it can be stated that reduced intestinal blood flow leads to ischemia and hypoxia of the villous tips. Reperfusion may lead to further mucosal injury. During this period oxygen free radicals and their derivates seem to play an essential role. Xanthine oxidase is thought to be the major source of these radicals in the small intestine. During ischemia ATP is catabolized to hypoxanthine, which is enzymatically transformed to xanthine, a process generating oxygen free radicals. Moreover oxygen free radicals seem to be produced by activated neutrophilic granulocytes. At present, only hypotheses exist concerning the interactions between granulocytes and these radicals. The mechanism of injury produced by oxygen free radicals is based on the peroxidation of the lipid components of the cellular membrane system. The small intestine represents a very vulnerable shock organ: apart from its very important nutritive functions, it provides the necessary barrier between the intestinal pool of endotoxin and the circulation. The loss of these vital functions due to ischemic lesions dramatically worsens the chances for the patient to survive. Therefore, it is necessary to develop therapeutic principles to maintain or restore intestinal function in shock.