title: Reperfusion injury after intestinal ischemia.
abstract: OBJECTIVE
  Review the histologic and pathophysiologic alterations seen after intestinal ischemia and reperfusion.
  
  
  METHODS
  Current literature review.
  
  
  METHODS
  The most pertinent, current, and representative articles describing results from both animal and human investigations are utilized and discussed.
  
  
  RESULTS
  Postischemic intestinal tissue damage appears to be due to the formation of oxygen radicals and the activation of phospholipase A2. The initial source of oxygen radicals seems to be the hypoxanthine-xanthine oxidase system. Oxygen radicals react directly with poly-unsaturated fatty acids, leading to lipid peroxidation within the cell membranes. Indirectly, the radicals trigger the accumulation of neutrophils within the affected tissue initiating inflammatory processes that lead to severe mucosal lesions. Similarly, phospholipase A2 also initiates postischemic mucosal lesions. Phospholipase A2 is a hydrolytic enzyme capable of increasing formation of cytotoxic lysophospholipids within the tissue. Enhanced activity of phospholipase A2 also stimulates the production of prostaglandins and leukotrienes. Various substances (superoxide dismutase, catalase, dimethyl sulfoxide, allopurinol, and deferoxamine, etc.) are able to detoxify oxygen radicals or inhibit the mechanisms leading to their enhanced generation, thus attenuating the postischemic lesions of the mucosa.
  
  
  CONCLUSIONS
  Oxygen radicals and the activation of phospholipase A2 during reperfusion seem to be instrumental for the development of hemorrhagic mucosal lesions after intestinal ischemia. Radical scavengers and phospholipase A2 inhibitors may prevent reperfusion damage of the intestine, even when the treatment starts during ischemia but before reperfusion.
authors.affiliation: Department of General Surgery, University of Ulm, FRG.
authors.forename: M H
authors.initials: MH
authors.lastname: Schoenberg
authors.forename: H G
authors.initials: HG
authors.lastname: Beger
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D002415:Cats; D004195:Disease Models, Animal; D016166:Free Radical Scavengers; D005609:Free Radicals; D005734:Gangrene; D006471:Gastrointestinal Hemorrhage / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D007042:Hypoxanthines / Q000502:physiology; D007249:Inflammation; D007422:Intestines / Q000098:blood supply*; D015289:Leukotrienes / Q000502:physiology; D015227:Lipid Peroxidation; D009504:Neutrophils / Q000502:physiology; D010741:Phospholipases A / Q000037:antagonists & inhibitors / Q000502:physiology; D054467:Phospholipases A2; D011453:Prostaglandins / Q000502:physiology; D051381:Rats; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D014969:Xanthine Oxidase / Q000502:physiology
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D005609:Free Radicals; D007042:Hypoxanthines; D015289:Leukotrienes; D011453:Prostaglandins; D017382:Reactive Oxygen Species; D014969:Xanthine Oxidase; D010741:Phospholipases A; D054467:Phospholipases A2