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OFRs are important mediators of tissue damage. However, extracellular OFR generation alone does not induce the typical enzymatic and morphologic changes of acute pancreatitis. Factors other than OFRs must be involved for triggering acute pancreatitis in vivo.

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.

given at an infusion rate of 0 6 ml/hour for periods ranging from 30 minutes to 12 hours. During infusion the rats had free access to pelleted food and water. After the infusion blood was sampled for plasma amylase and lipase measurements and pancreatic tissue samples were excised for light and electron microscopic 1138 on 10 May 2018 by guest. Protected by copyright.

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Oxygen radicals mediate an important step in the initiation of acute pancreatitis. These reactive oxygen metabolites are generated at an early stage of the disease. The source of the enhanced production of oxygen radicals, however, still remains unclear. Experimentally, the effectiveness of antioxidant treatment varies from one model to the other, the differences depending on the experimental model and not on the form of pancreatitis that was induced. In most studies, the experimental animals were pretreated before acute pancreatitis was induced. This does not mirror clinical reality because patients are admitted to the hospital after the onset of the disease. It was shown in cerulein-induced pancreatitis, however, that scavenger treatment also mitigated the pancreatic tissue damage after induction of acute pancreatitis. Moreover, antioxidant treatment also attenuated the extrapancreatic complications, thus improving the final outcome of the disease. Initial indirect observations also suggest that in human acute, acute recurrent, and chronic pancreatitis, oxygen free radicals are generated and add to the damage. Concomitantly, these patients suffer from a severe depletion of oxidative stress. Whether or not this disbalance is instrumental in the development and course of disease remains unanswered. Supplementation with antioxidants that are deficient in patients with acute pancreatitis might be a feasible option to the present therapy to avoid extrapancreatic complications. Well-defined, controlled clinical trials involving patients suffering from acute pancreatitis are therefore needed to validate the role of oxygen radicals in this disease.

Our trial shows that CWEPs are effective at reducing the incidence of SSIs in elective and clean or clean-contaminated open abdominal surgery.