title: Role of hypertriglyceridemia in the pathogenesis of experimental acute pancreatitis in rats.
abstract: CONCLUSIONS
  The pancreatic damage initiated via different pathogenetic pathways can be increased by triglycerides. Thus, triglycerides seem to play an important role in the pathogenesis of acute pancreatitis.
  
  
  BACKGROUND
  Lipolytic enzymes and their substrates may play a role in the pathogenesis of acute necrotizing pancreatitis. We investigated, therefore, whether triglycerides alter the course of acute pancreatitis in three experimental models of rats.
  
  
  METHODS
  1. Edematous acute pancreatitis induced by repeated sc injections of cerulein; 2. Necrotizing acute pancreatitis by retrograde duct injection of sodium taurocholate; and 3. Pancreatic edema by ligation of: a. The bile duct at the liver hilus; b. The common bile/pancreatic duct close to the duodenal wall; or c. A combination of a. and b. Six hours later, rats were sacrificed and the isolated perfused pancreas prepared. The pancreases were perfused with either HEPES/Ringer/HAES alone or in combination with various concentrations of triglycerides (1-5% wt/vol). The activities of lipase and amylase in the portal venous effluents were regarded as a marker of pancreatic injury. In addition, the pancreases were evaluated by light microscopy.
  
  
  RESULTS
  In both cerulein and taurocholate acute pancreatitis, amylase/lipase activities were significantly higher compared to controls during 45 min of perfusion. In both models, addition of triglycerides caused a dose-dependent marked elevation of enzymes. Ligation (a) did not cause any rise in enzymes in the venous effluent; triglycerides had no effect. Ligation (b) or (c) caused a significant increase of pancreatic enzymes, which was further increased by triglycerides. Histology showed various degrees of severity of tissue damage depending on the model used. The additional damaging effect of a 45-min perfusion with triglycerides, however, could not be detected by histology.
authors.affiliation: Department of Internal Medicine II, University of Leipzig, Germany.
authors.forename: W
authors.initials: W
authors.lastname: Kimura
authors.forename: J
authors.initials: J
authors.lastname: Mössner
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000378:metabolism; D000818:Animals; D002108:Ceruletide; D005765:Gastrointestinal Agents; D015228:Hypertriglyceridemia / Q000201:enzymology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008049:Lipase / Q000378:metabolism; D008297:Male; D010179:Pancreas / Q000201:enzymology; D010195:Pancreatitis / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013656:Taurocholic Acid; D014280:Triglycerides / Q000502:physiology
chemical_list: D005765:Gastrointestinal Agents; D014280:Triglycerides; D013656:Taurocholic Acid; D002108:Ceruletide; D008049:Lipase; D000681:Amylases