The role of inflammatory mediators in severe acute pancreatitis and regulation of glucocorticoids
Wang, Z.-F.; Pan, C.-E.; Lu, Y.; Liu, S.-G.; Zhang, G.-J.; Zhang, X.-B.
Hepatobiliary and Pancreatic Diseases International Hbpd Int 2(3): 458-462
2003
ISSN/ISBN: 1499-3872 PMID: 14599960 Document Number: 556371
To investigate the effect of glucocorticoids on systemic inflammatory mediator release in rats with acute pancreatitis and the outcome of dexamethasone in treatment of acute pancreatitis. Sixty-eight Wistar rats were divided into sham, acute pancreatitis, and treatment (intravenous dexamethasone 0.5 mg/kg) groups. Experimental acute pancreatitis was induced by the injection of 5% sodium taurocholate (0.1 ml/100 mg body weight) into the pancreatic-biliary duct. The blood samples were obtained and examined for 6-keto-PGI1alpha, TXB2 and IL-6 postoperatively at 3, 6 and 12 hours, respectively. The pancreatic samples were evaluated by a blinded method. Twelve-hour survival rate was determined and compared between the groups. The high serum concentrations of 6-keto-PGI1alpha, TXB2 and IL-6 were noted in the rats with acute pancreatitis associated with pancreatic hemorrhage and necrosis. Their 12-hour survival rate was 42.9%. The rats in the treatment group survived with significantly reduced serum concentrations of 6-keto-PGI1alpha, TXB2 and IL-6 (P<0.05). Their pancreatic morphology was normal. Dexamethasone may reduce the serum concentration of 6-keto-PGI1alpha, TXB2, and IL-6, and the severity of acute pancreatitis while increasing the survival rate of rats with acute pancreatitis.