cytochrome-c-t and Postoperative-Complications

Postoperative intra-abdominal adhesion formation remains a major surgical problem. Surgery induces an inflammatory reaction, which is responsible for adhesion formation. Neutrophils and their oxygen-free radicals are key mediators in the early post-operative inflammatory response. The present study evaluates the effect of either blocking the influx of neutrophils or its products by scavenging oxygen-free radicals on adhesion formation.. Reproducible rat models were used to induce post-surgical intra-abdominal adhesions. In the first experiment anti-neutrophil serum (ANS) was used to prevent neutrophils from entering the peritoneal cavity after surgery. In a second experiment superoxide dismutase (SOD), catalase, and mannitol were tested, to scavenge the superoxide, hydrogen peroxide, and hydroxyl radicals, respectively.. In positive control groups 69 to 76% of the area of interest contained adhesions. In all experimental groups, except for mannitol, a significant reduction in post-surgical adhesion formation could be achieved. ANS reduced adhesion formation by 38% (P < 0.001) and SOD/catalase by 42% (P < 0.01). Mannitol could not reduce adhesion formation.. Intra-abdominal influx of neutrophils after surgical peritoneal trauma plays an important role in post-operative adhesion formation. Preventing the intra-abdominal influx of neutrophils in the early post-operative inflammatory reaction can reduce adhesion formation, but an even more selective approach, by scavenging its products, proved as efficient.

Topics: Animals; Apoptosis; Cell Division; Cytochromes c; Disease Models, Animal; Female; Humans; L-Lactate Dehydrogenase; Neutrophils; Omentum; Plasminogen Activator Inhibitor 1; Postoperative Complications; Rats; Rats, Inbred Strains; Reactive Oxygen Species; Tissue Adhesions; Tissue Plasminogen Activator