W Kimura1, J Mössner. 1. Department of Internal Medicine II, University of Leipzig, Germany.
Abstract
CONCLUSION: 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.
CONCLUSION: 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: R Mantke; D Schubert; C Röcken; I Paege; W Halangk; B Peters; H Lippert; H-U Schulz Journal: Langenbecks Arch Surg Date: 2008-08-09 Impact factor: 3.445