Hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in the rat.
Department of Visceral and Transplantation Surgery, University of Berne, Switzerland.
BACKGROUND--Serum triglyceride concentrations higher than 10 to 20 mmol/l are probably a risk factor for developing acute pancreatitis in humans. AIMS--To therefore analyse the influence of hyperlipaemia on the course of acute oedematous and acute necrotising pancreatitis in rats. SUBJECTS--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. CONCLUSION--This study shows that hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in rats.
This article has been cited by other articles:
-
Wang, Y, Sternfeld, L, Yang, F, Rodriguez, J A, Ross, C, Hayden, M R, Carriere, F, Liu, G, Hofer, W, Schulz, I
(2009). Enhanced susceptibility to pancreatitis in severe hypertriglyceridaemic lipoprotein lipase-deficient mice and agonist-like function of pancreatic lipase in pancreatic cells. Gut
58: 422-430
[Abstract] [Full Text] -
Wildi, S., Kleeff, J., Mayerle, J., Zimmermann, A., Bottinger, E. P, Wakefield, L., Buchler, M. W, Friess, H., Korc, M.
(2007). Suppression of transforming growth factor {beta} signalling aborts caerulein induced pancreatitis and eliminates restricted stimulation at high caerulein concentrations. Gut
56: 685-692
[Abstract] [Full Text] -
Sakai, H., Masada, Y., Horinouchi, H., Ikeda, E., Sou, K., Takeoka, S., Suematsu, M., Takaori, M., Kobayashi, K., Tsuchida, E.
(2004). Physiological Capacity of the Reticuloendothelial System for the Degradation of Hemoglobin Vesicles (Artificial Oxygen Carriers) after Massive Intravenous Doses by Daily Repeated Infusions for 14 Days. J. Pharmacol. Exp. Ther.
311: 874-884
[Abstract] [Full Text] -
Shrikhande, S., Friess, H., Issenegger, C., Martignoni, M. E., Yong, H., Gloor, B., Yeates, R., Kleeff, J., Büchler, M. W.
(2000). Fluconazole Penetration into the Pancreas. Antimicrob. Agents Chemother.
44: 2569-2571
[Abstract] [Full Text]
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
