Hammond J B, Mann N S
Am J Dig Dis. 1977 Mar;22(3):182-8. doi: 10.1007/BF01072274.
Experimental pancreatitis (PT) is induced by proximal and distal duodenal closure in the bile-duct-ligated dog, by causing duodeno-pancreatic reflux of lumenal secretions. It has been postulated that trypsin and enterokinase (EK) in the secretions activate trypsinogen within the pancreas, producing PT. There is supporting evidence for trypsin, but EK has not previously been investigated. To determine whether EK alone could cause PT, we injected saline suspensions of partially purified EK, and other test materials, into the duct of Wirsung of dogs and after 24 hr examined their pancreases and estimated the increment in serum amylase. Following 0.5% EK, both PT and hyperamylasemia (HA) ensued; HA without PT occured when EK was inactivated by heat, administered with trypsin inhibitor (TI), or administered in more dilute solution. Injection of TI or of hog gastric mucin likewise leads to HA but not to PT. It is concluded that the PT observed was due to EK activity, and that therefore EK could contribute to the production of PT observed was due to EK activity, and that therefore EK could contribute to the production of PT in the closed-duodenal-loop model. The HA observed in the absence of PT is unexplained but appears to be related to the colloidal properties of the materials injected.
实验性胰腺炎（PT）是通过结扎胆管的犬近端和远端十二指肠闭合，导致肠腔分泌物十二指肠-胰腺反流而诱发的。据推测，分泌物中的胰蛋白酶和肠激酶（EK）激活胰腺内的胰蛋白酶原，从而引发PT。有证据支持胰蛋白酶的作用，但此前尚未对EK进行研究。为了确定单独的EK是否会导致PT，我们将部分纯化的EK和其他测试物质的盐溶液注入犬的胰管，24小时后检查它们的胰腺并估计血清淀粉酶的增量。注射0.5%的EK后，PT和高淀粉酶血症（HA）均出现；当EK被加热灭活、与胰蛋白酶抑制剂（TI）一起给药或用更稀的溶液给药时，出现HA但无PT。注射TI或猪胃粘蛋白同样会导致HA，但不会导致PT。得出的结论是，观察到的PT是由于EK活性，因此EK可能在十二指肠闭合环模型中促成PT的产生。在没有PT的情况下观察到的HA无法解释，但似乎与注射物质的胶体性质有关。
