title: Free radicals and pathogenesis during ischemia and reperfusion of the cat small intestine.
abstract: OBJECTIVE
  In spite of the interest in free radicals as mediators of ischemic damage, most information on these species in biological systems is derived from indirect measurements. Our aim was to obtain more direct information concerning sources of free radical production during ischemia and reperfusion.
  
  
  METHODS
  We have performed simultaneous measurement of radical generation, purine metabolites, reduced glutathione, neutrophil infiltration and morphological appearance in the cat small intestine in vivo during 60 minutes of ischemia followed by 60 minutes of reperfusion.
  
  
  RESULTS
  Radical formation increased abruptly on reperfusion and remained elevated in untreated animals. Inhibition by a monoclonal antibody (IB4) against the neutrophil and by allopurinol treatment was paralleled by improvement of biochemical and morphological parameters. The radicals detected during reperfusion could be divided into one component arising directly from the neutrophils, one due to the xanthine oxidase reaction, and one unknown source.
  
  
  CONCLUSIONS
  Neutrophils are a major source of radical production during reperfusion after ischemia. Radicals formed in the xanthine oxidase reaction seem to function as a primer for the neutrophils. The nonsignificant linear correlation between radical formation and morphological appearance suggests that factors other than free radicals are important for the development of intestinal damage after a period of ischemia.
authors.affiliation: Department of Physiology, University of Göteborg, Sweden.
authors.forename: U A
authors.initials: UA
authors.lastname: Nilsson
authors.forename: M H
authors.initials: MH
authors.lastname: Schoenberg
authors.forename: A
authors.initials: A
authors.lastname: Aneman
authors.forename: B
authors.initials: B
authors.lastname: Poch
authors.forename: S
authors.initials: S
authors.lastname: Magadum
authors.forename: H G
authors.initials: HG
authors.lastname: Beger
authors.forename: O
authors.initials: O
authors.lastname: Lundgren
mesh_terms: D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D001706:Biopsy; D002415:Cats; D005260:Female; D019271:Hypoxanthine; D007042:Hypoxanthines / Q000378:metabolism; D007413:Intestinal Mucosa / Q000473:pathology; D007421:Intestine, Small / Q000098:blood supply* / Q000473:pathology; D007511:Ischemia / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009504:Neutrophils / Q000276:immunology; D009195:Peroxidase / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D007042:Hypoxanthines; D017382:Reactive Oxygen Species; D019271:Hypoxanthine; D000493:Allopurinol; D009195:Peroxidase; D014969:Xanthine Oxidase