title: Intestinal mucosal injury during porcine faecal peritonitis.
abstract: OBJECTIVE
  To assess the incidence of intestinal mucosal injury during faecal peritonitis in pigs, the relation of such lesions to haemodynamic variables, intramucosal pH (pHi), and endothelial adherence of polymorphonuclear leucocytes (PMNs).
  
  
  METHODS
  Experimental laboratory study.
  
  
  METHODS
  University department of surgery, Sweden.
  
  
  METHODS
  57 Juvenile pigs.
  
  
  METHODS
  Pigs had faecal peritonitis induced (n = 39) or a sham procedure (n = 18). In addition, 15 animals were pretreated with the monoclonal CD18 receptor antibody IB4 before induction of peritonitis with the aim of preventing tissue accumulation of PMNs.
  
  
  METHODS
  Development of mucosal lesions and correlation with haemodynamic variables.
  
  
  RESULTS
  17/18 (94%) of control animals had normal mucosa. The incidence of mucosal lesions in animals with faecal peritonitis was 56%. Animals with severe mucosal injury (grade 4-5) had significantly lower mean arterial pressure, cardiac index, and pHi during the last hour of the experiment compared with animals without mucosal lesions. Pretreatment with IB4 did not prevent the development of intestinal mucosal injuries. Intramucosal pH decreased during sepsis and was not affected by IB4.
  
  
  CONCLUSIONS
  Severe intestinal mucosal injury is associated with arterial hypotension, low cardiac index, and low pH. Neither the mucosal injury nor the reduction in pHi seen during porcine faecal peritonitis seemed to be leucocyte-related phenomena.
authors.affiliation: Department of Surgery, University Hospital, Uppsala, Sweden.
authors.forename: S
authors.initials: S
authors.lastname: Wollert
authors.forename: J
authors.initials: J
authors.lastname: Antonsson
authors.forename: B
authors.initials: B
authors.lastname: Gerdin
authors.forename: C
authors.initials: C
authors.lastname: Lundberg
authors.forename: I B
authors.initials: IB
authors.lastname: Rasmussen
authors.forename: U
authors.initials: U
authors.lastname: Haglund
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001794:Blood Pressure; D018821:CD18 Antigens / Q000276:immunology; D002302:Cardiac Output; D002448:Cell Adhesion; D004727:Endothelium / Q000473:pathology; D005243:Feces; D005260:Female; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009504:Neutrophils / Q000473:pathology; D010538:Peritonitis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D013552:Swine
chemical_list: D000911:Antibodies, Monoclonal; D018821:CD18 Antigens