The role of inflammatory mediators in severe acute pancreatitis and regulation of glucocorticoids

<正> OBJECTIVE: To investigate the effect of glucocorticoids on systemic inflammatory mediator release inrats with acute pancreatitis and the outcome of dexamethasone in treatment of acute pancreatitis.METHODS: 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 theinjection of 5% sodium taurocholate （0.1 ml/100 mg body weight） into the pancreatic-biliary duct. ThebIood samples were obtained and examined for 6-keto-PGI1α, TXB2 and IL-6 postoperatively at 3,6 and12 hours, respectively. The pancreatic samples were evaluated by a blinded method. Twelve-hour survivalrate was determined and compared between the groups.RESULTS: The high serum concentrations of 6-keto-PGI1α, TXB2 and IL-6 were noted in the rats withacute pancreatitis associated with pancreatic hemorrhage and necrosis. Their 12-hour survival rate was42.9%. The rats in the treatment group survived with significantly reduced serum concentrations of6-keto-PGI1α, TXB2 and IL-6 （P<0.05）. Their pancreatic morphology was normal.CONCLUSION: Dexamethasone may reduce the serum concentration of 6-keto-PGI1α, TXB2, and IL-6,and the severity of acute pancreatitis while increasing the survival rate of rats with acute pancreatitis.