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暴发性急性胰腺炎动物模型的建立 被引量:1

Establishment of animal models of fulminant acute pancreatitis.
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摘要 目的建立暴发性急性胰腺炎模型,为研究其发病机制提供实验模型。方法30只SD大鼠随机分为假手术组、ANP组、LPS加重组、LPS+BPDL(胆胰管结扎)组和LPS+GdCl3组,各6只。于制模术后6h观察各组最大采血量、腹水量及血清谷丙转氨酶、肌酐、淀粉酶、TNF-α的含量和腹水淀粉酶、TNF-α的含量,并对胰腺、肺脏、肝脏和肾脏做病理检查。结果LPS加重组、LPS+BPDL组的腹水量、谷丙转氨酶、肌酐、淀粉酶、TNF-α均较ANP组、假手术组明显升高;而最大采血量明显减少;肺脏和肝脏病理分值显著升高(均P〈0.05或0.01)。LPS+BPDL组较LPS加重组的病情严重程度更重。LPS+GdCl3组较LPS加重组的有效循环血量和肝肾功能明显改善,肺脏组织病理学改变明显减轻。结论在ANP基础上从胆胰管内加注内毒素可产生较ANP更为严重的病理损伤,可以作为一种暴发性急性胰腺炎的模型。 Objective To investigate the pathogenesis of fulminant acute pancreatitis (FAP) by establishing relevant animal models. Methods Thirty SD rats were divided into 5 groups, which were the sham operation group, ANP group, LPS group, LPS+BPDL (ligation of bilio-pancreatic duct) group and LPS + GdCl3 group. At the 6th hour after induction, maximal intravenous dose volumes, amount of ascites, serum glutamic pyruvic transaminase, creatinine, serum amylase, TNF-α, as well as amylase and TNF-α in ascites were recorded. Pathological examination was conducted in pancreas, lung, liver and kidney tissues. Results The increment of amount of ascites, glutamic pyruvic transaminase, creatinine, serum amylase and TNF-α in LPS group, LPS + BPDL group were significantly higher when compared with those in the sham operation group, ANP group. However, the maximal intravenous dose volumes decreased significantly. The pathological scores in lung and liver tissues increased significantly (P 〈 0.05 or 0.01). The severity of ANP in LPS + BPDL group was more pronounced than that in LPS group. LPS + GdCl3 group's circulation volume and liver, kidney function significantly improved and the pathological injury of the lung were significantly reduced. Conclusions Retrograde biliary injection of endotoxin may cause more severe pathological injury and could be used for the establishment of animal models of FAP.
出处 《胰腺病学》 2007年第5期297-300,共4页 Chinese JOurnal of Pancreatology
基金 上海市教育局课题基金资助(02BK11)
关键词 胰腺炎 急性坏死性 胆道 内毒素类 KUPFFER细胞 Pancreatitis, acute necrotizing Biliary tract Endotoxins Kupffer cell
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