| 1 | The role of inflammatory mediators in severe acute pancreatitis and regulation of glucocorticoids显示文摘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. | Zi-Fa Wang Cheng-En Pan Yi Lu Shao-Gao Liu Guan-Jun Zhang Xue-Bin Zhang the Departments of Surgery and Pathology First Hospital, Xi’an Jiaotong University, Xi’an 710061, China the Department of Surgery, University of Pittsburgh, NW607, Montefiore University Hospital, 3459 Fifth Avenue, Pittsburgh, PA 15213, USA | 2003 | Hepatobiliary & Pancreatic Diseases International2003，2，3： | 3 |
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