Proteases and protease inhibitors in taurocholate-induced acute pancreatitis in rats.

P Kruse, E Hage, A Lasson
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引用次数: 15

Abstract

Conclusion: Taurocholate-induced acute pancreatitis (AP) in the rat mimics early necrotizing human pancreatitis. Protease activation and protease inhibitor consumption occur consistent with a two-stage development, and contact-phase activation is a possible primary event in this model.

Background: Proteases and protease inhibitors have been indicated to play an important role in both human and experimental acute pancreatitis, although little is known about them in rats.

Methods: Three percent sodium taurocholate was infused into the bilio-pancreatic duct to induce AP, and over 0-72 h we measured lipase, amylase, albumin, prekallikrein, factor X, alpha-1-macroglobulin, alpha-2-antiplasmin, antithrombin III, alpha-1-protease inhibitor, and C1-esterase inhibitor (all in plasma) and histologic and macroscopic findings.

Results: A severe necrotizing, nonlethal, AP was induced with an early increase in plasma lipase and alpha-amylase activity levels and peritoneal exudate followed by a return to near control levels after 72 h. Histologic score and pancreatic wet weight ratio increased initially and remained high during the observation period. The protease inhibitors C1-esterase inhibitor, alpha-2-antiplasmin, and antithrombin III decreased early, within 0-6 h, whereafter levels normalized. The protease inhibitors alpha-1-macroglobulin and alpha-1-protease inhibitor later gradually decreased over the 72 h.

牛磺胆酸诱导大鼠急性胰腺炎的蛋白酶和蛋白酶抑制剂。
结论:牛磺酸胆碱诱导的大鼠急性胰腺炎(AP)与早期坏死性人胰腺炎相似。蛋白酶激活和蛋白酶抑制剂的消耗与两个阶段的发展相一致,接触阶段的激活可能是该模型中的主要事件。背景:蛋白酶和蛋白酶抑制剂已被证明在人类和实验性急性胰腺炎中发挥重要作用,尽管对它们在大鼠中的作用知之甚少。方法:将3%牛磺酸胆酸钠注入胆道胰管诱导AP,在0-72 h内测定脂肪酶、淀粉酶、白蛋白、前钾化酶、X因子、α -1巨球蛋白、α -2抗纤溶酶、抗凝血酶III、α -1蛋白酶抑制剂和c1酯酶抑制剂(均在血浆中)的组织学和宏观表现。结果:严重坏死性非致死性AP,早期血浆脂肪酶和α -淀粉酶活性水平和腹膜渗出液升高,72小时后恢复到接近对照水平。组织学评分和胰腺湿重比最初升高,并在观察期间保持较高水平。蛋白酶抑制剂c1 -酯酶抑制剂,α -2-抗纤溶酶和抗凝血酶III在0-6小时内早期下降,此后水平恢复正常。蛋白酶抑制剂α -1-巨球蛋白和α -1-蛋白酶抑制剂在72 h内逐渐降低。
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