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 occurred 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 in the closed-duodenalloop model. The HA observed in the absence of PT is unexplained but appears to be related to the colloidal properties of the materials injected.
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