The Toxicity of the Products of Pancreatic and Gastric Digestion. 20

Abstract

The most widely accepted theory regarding the etiology and pathogenesis of acute pancreatitis may be briefly stated as follows: A premature or intra-pancreatic activation of the trypsinogen of pancreatic juice is caused by the entrance of bile or duodenal juice into the pancreatic ducts or as a result of trauma or infection. It is then further assumed that the active trypsin so produced digests away the gland, that the end products of this tryptic digestion of pancreas are toxic, that they are absorbed into the blood stream and occasion a fatal toxemia. Ellis and Dragstedt 1 found that the uncontaminated liver of normal dogs contains bacteria in a very high percentage of cases and that the toxemia resulting from liver autolysis in vivo is dependent upon the activity of these bacteria in the presence of necrotic liver. By a similar technique to be reported in detail elsewhere we have found that the normal uncontaminated pancreas of healthy adult dogs also regularly contains bacteria and that the fatal toxemia resulting from the intraperitoneal autolysis of pancreas is likewise in large measure dependent upon the activity of these bacteria in the presence of necrotic pancreas. In this connection it has occurred to us that a reinvestigation of the toxicity of gastric and pancreatic juice and of the end products of the disintegration of body tissue produced by these juices in the strict absence of bacterial activity would be desirable. The present experiments were designed to determine the toxicity of the end products of gastric and pancreatic digestion.

Gastric juice was obtained from a Pavlow pouch and fresh active pancreatic juice from a specially devised fistula, previously described. 2 These were sterilized by passage through a Berkefeld filter (N).