title: The role of neutrophils and oxygen free radicals in post-operative adhesions.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of General Surgery, ErasmusMC, Rotterdam, The Netherlands. sandertenraa@hotmail.com
authors.forename: Sander
authors.initials: S
authors.lastname: ten Raa
authors.forename: M Petrousjka
authors.initials: MP
authors.lastname: van den Tol
authors.forename: Wim
authors.initials: W
authors.lastname: Sluiter
authors.forename: Leo J
authors.initials: LJ
authors.lastname: Hofland
authors.forename: Casper H J
authors.initials: CH
authors.lastname: van Eijck
authors.forename: Hans
authors.initials: H
authors.lastname: Jeekel
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D045304:Cytochromes c / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009504:Neutrophils / Q000166:cytology / Q000276:immunology* / Q000378:metabolism*; D009852:Omentum / Q000166:cytology; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011183:Postoperative Complications / Q000276:immunology / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D017382:Reactive Oxygen Species / Q000378:metabolism*; D000267:Tissue Adhesions / Q000276:immunology* / Q000378:metabolism*; D010959:Tissue Plasminogen Activator / Q000378:metabolism
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D017382:Reactive Oxygen Species; D045304:Cytochromes c; D007770:L-Lactate Dehydrogenase; D010959:Tissue Plasminogen Activator