title: Hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in the rat.
abstract: BACKGROUND
  Serum triglyceride concentrations higher than 10 to 20 mmol/l are probably a risk factor for developing acute pancreatitis in humans.
  
  
  OBJECTIVE
  To therefore analyse the influence of hyperlipaemia on the course of acute oedematous and acute necrotising pancreatitis in rats.
  
  
  METHODS
  Male Wistar rats were used in all experiments.
  
  
  METHODS
  Six different groups of animals were used: two groups without pancreatitis (controls), two with acute oedematous pancreatitis, and two with acute necrotising pancreatitis. One group from each pair was treated with Triton WR 1339, which induces endogenous hyperlipaemia. Blood samples were taken from all subjects to measure triglyceride, cholesterol, amylase, and lipase. Pancreatic tissue samples were taken and the degree of pancreatic damage was judged microscopically.
  
  
  RESULTS
  In the control groups no significant changes occurred, either in serum enzyme activities or in histology. The hyperlipaemic subgroup of animals with acute oedematous pancreatitis developed significantly higher (p < 0.001) serum amylase activities and a greater degree of histological damage (p < 0.01) than the animals of the non-hyperlipaemic acute oedematous pancreatitis group. In the animals with necrotising pancreatitis, serum lipase activity and the histological degree of pancreatic damage were significantly higher in the hyperlipaemic animals than in the non-hyperlipaemic animals.
  
  
  CONCLUSIONS
  This study shows that hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in rats.
authors.affiliation: Department of Visceral and Transplantation Surgery, University of Berne, Switzerland.
authors.forename: B
authors.initials: B
authors.lastname: Hofbauer
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: A
authors.initials: A
authors.lastname: Weber
authors.forename: K
authors.initials: K
authors.lastname: Baczako
authors.forename: P
authors.initials: P
authors.lastname: Kisling
authors.forename: M
authors.initials: M
authors.lastname: Schilling
authors.forename: W
authors.initials: W
authors.lastname: Uhl
authors.forename: C
authors.initials: C
authors.lastname: Dervenis
authors.forename: M W
authors.initials: MW
authors.lastname: Büchler
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood*; D000818:Animals; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D018450:Disease Progression; D004487:Edema / Q000097:blood / Q000209:etiology / Q000473:pathology; D006949:Hyperlipidemias / Q000139:chemically induced / Q000150:complications*; D008049:Lipase / Q000097:blood*; D008297:Male; D009336:Necrosis; D010195:Pancreatitis / Q000097:blood / Q000209:etiology* / Q000473:pathology; D011092:Polyethylene Glycols / Q000009:adverse effects; D051381:Rats; D017208:Rats, Wistar; D013501:Surface-Active Agents / Q000009:adverse effects; D014280:Triglycerides / Q000097:blood
chemical_list: D013501:Surface-Active Agents; D014280:Triglycerides; D011092:Polyethylene Glycols; D002784:Cholesterol; D008049:Lipase; D000681:Amylases; C016811:tyloxapol