摘要目的本文探讨急性坏死性胰腺炎多器官损伤机制,并对防治ANP的全身炎症反应综合征和多器官功能障碍综合征及其治疗策略进行研究.方法经胰胆管逆行注射3.5%牛磺胆酸钠2.5?ml/kg建立鼠ANP模型,测定血清IL-6、IL-8、IL-10、TNFα、淀粉酶、内毒素和白蛋白.胰腺、肝、心、肺和肾病理观察及细胞超微结构观察,TNFα mRNA分子转录水平的RT-PCR分析,探讨生长抑素和生长激素治疗作用.结果 ANP的发生和发展伴有炎性介质的明显升高,与ANP和MODS的发展呈正相关.生长抑素和生长激素对抑制炎性介质的释放和TNFα mRNA过度表达有协同作用,同时亦表明肝脏在ANP中对预防宿主多器官衰竭有重要作用.结论 TNFα mRNA的高度表达在ANP的进展中至关重要,生长抑素和生长激素的联合治疗对防治ANP的MODS的发生和防治有重要作用.

abstractsAbstract:Objective To determine the role of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), and evaluate the progress from SIRS to MODS and the therapeutic strategies for acute necrotizing pancreatitis (ANP).Methods Rat ANP models were made by retrograde injection of 3.5% sodium taurocholate 2.5?ml/kg into the pancreatic duct. Serum interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNFα), amylase, endotoxin, and albumin were examined. The morphology and pathology of the pancreas, liver, lung, kidney and heart after ANP were observed. Finally, TNFα mRNA in the liver, lung, kidney and heart after ANP were observed by reverse transcriptase-polymerase chain reactions, and the efficiency of somatostatin and growth hormone were also observed in this experiment.Results ANP led to remarkable elevation of the inflammatory mediators which were positively correlated with the development of ANP and MODS. Somatostatin and growth hormone inhibited inflammatory mediators and TNFα mRNA overexpressions, reduced the risk of MODS, corrected hypoalbuminemia, reversed negative nitrogen balance, and controlled the reduction of cell groups with functions and reasonably intervened SIRS caused by ANP.Conclusion TNFα mRNA plays an important role in ANP progression. The amelioration of ANP by combination treatment with somatostatin and growth hormone leads to the reduction of complications and marked increase in survival.