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胆汁和胰液排除会激活腺泡应激激酶并加重胆石性胰腺炎。

Bile and pancreatic juice exclusion activates acinar stress kinases and exacerbates gallstone pancreatitis.

作者信息

Samuel Isaac

机构信息

Department of Surgery, University of Iowa Roy J. and Lucille A. Carver College of Medicine and Veterans Administration Medical Center, Iowa City, Iowa 52242, USA.

出版信息

Surgery. 2008 Mar;143(3):434-40. doi: 10.1016/j.surg.2007.06.004. Epub 2007 Dec 21.

Abstract

Bile and pancreatic juice exclusion from gut activates acinar stress kinases and exacerbates gallstone pancreatitis as evidenced by the ameliorating effects of replacement therapy in an experimental model of duct ligation-induced acute pancreatitis. In the early stages of gallstone pancreatitis, bile-pancreatic juice cannot enter the gut. Enteral exclusion worsens pancreatitis by causing feedback hyperstimulation of the exocrine pancreas that activates acinar cell stress kinases. Investigations using a unique surgical model, the Donor Rat Model, showed that duodenal replacement of bile-pancreatic juice in rats with duct ligation attenuates pancreatic stress kinase activation, reduces pancreatic cytokine production, and ameliorates pancreatic morphologic changes. These findings suggest that exclusion-induced acinar hyperstimulation, in the presence of duct obstruction, exacerbates acute pancreatitis via stress kinase activation. Although acinar hyperstimulation has often been implicated in the pathogenesis of acute pancreatitis, the lack of supporting evidence remains a conspicuous void. The proposed hypothesis draws on fresh evidence to present a new paradigm that reexamines the role of exocrine pancreatic hyperstimulation in gallstone pancreatitis pathogenesis.

摘要

在胆管结扎诱导的急性胰腺炎实验模型中,替代疗法具有改善作用,这表明胆汁和胰液从肠道排除会激活腺泡应激激酶并加重胆石性胰腺炎。在胆石性胰腺炎的早期阶段,胆汁-胰液无法进入肠道。肠内排除通过引起外分泌胰腺的反馈性过度刺激而使胰腺炎恶化,这种过度刺激会激活腺泡细胞应激激酶。使用独特的手术模型——供体大鼠模型进行的研究表明,对胆管结扎大鼠进行十二指肠胆汁-胰液替代可减弱胰腺应激激酶的激活,减少胰腺细胞因子的产生,并改善胰腺形态学变化。这些发现表明,在存在胆管梗阻的情况下,排除诱导的腺泡过度刺激通过应激激酶激活加剧急性胰腺炎。尽管腺泡过度刺激常常被认为与急性胰腺炎的发病机制有关,但缺乏支持证据仍然是一个明显的空白。提出的假说利用新证据提出了一个新的范例,重新审视外分泌胰腺过度刺激在胆石性胰腺炎发病机制中的作用。

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