Many of the factors in the pathogenesis and experimental production of acute pancreatitis are conflicting and controversial. It is generally conceded that interstitially extravasated, active trypsin in the pancreas plays a dominant role.1,2 Evidence further indicates that if, in addition, ductal obstruction or ischemia supervenes, necrotic or hemorrhagic pancreatitis is likely to ensue.1-4 The pivotal issues seem to be (1) the mechanism by which trypsin or trypsinogen is extravasated, (2) whether trypsinogen itself can cause pancreatitis, and (3) the manner in which trypsinogen is activated.
The majority of investigators have utilized ductal perfusion of bile or pancreatic juice.1,3 Stein and co-workers have produced hemorrhagic pancreatitis by injection of trypsin into the dog's pancreaticoduodenal artery and ligation of the pancreatic ducts. Hosie and Ziffren5 have implicated collagenase, normally contained in pancreatic juice, as the initiator of pancreatitis. Since much of the experimental evidence indicating active trypsin as