The Production of Anomalous Pancreaticobiliary Ductal Union in Canine Models

Abstract

For the purpose of resolving the mechanism of the ill-effect of refluxed pancreatic juice, due to the anomalous pancreaticobiliary ductal union, canine models were produced. Mongrel adult dogs and puppies were used. Pancreatico-cholecystostomy was performed on 5 adult dogs and 5 puppies. Pancreatico-choledochostomy was performed on 10 adult dogs and 5 puppies. In both procedures, the cylindrical dilatation of the choledochus resulted. The pathological changes in the choledochus were very similar to the cylindrical choledochal dilatation in the human. Elastic fibers diminished universally and in some cases they vanished completely. The changes in the papilla of the bile duct were very slight. There were no cases with hardened papilla. The pathological changes were greater in the pancreatico-cholecystostomy. Enzymatic analysis of pancreatic juice in bile was very important in explaining the etiology. Amylase was proven to be very high throughout the cases, over 10,000 IU/1 by enzymatic assay. Trypsin and elastase were proven to be activated in pancreatico-cholecystostomy, naturally assuming the existence of enterokinase. They were aso proved to be activated in the pancreatico-choledochostomy, without the existence of enterokinase. Though the mechanism was not clear, the activated proteases were the actual cause of the ill-effect in this anomaly. Thus we have succeeded in producing the ideal animal models of the reflux of pancreatic juice into the bile duct in adult dogs and puppies.

Pancreaticobiliary Maljunction‐Associated Pancreatitis: An Experimental Study on the Activation of Pancreatic Phospholipase A2

“…It has been shown that in humans the existence of PBM results in an elevated amylase concentration in bile. Other pancreatic enzymes, such as trypsin and elastase, have also been shown to be in an activated state under such circumstances [23]. There is also evidence that no activation of trypsin ensued in vitro from simply allowing the enzyme to intermingle with bile, which normally contains no enterokinase.…”

Preliminary exploration of animal models of congenital choledochal cysts

“…Various animal models to simulate the disease process in humans have been used to investigate the pathogenesis of cystic and fusiform CCs. However, anastomosis of the pancreatic and biliary ducts, which allow pancreatic juice to enter the bile duct, only resulted in mild dilation of the common bile duct without cystic dilatation[ 4 ]. Moreover, even in large animal models, such as minipigs, no one was observed to have dilatation of the bile ducts[ 5 ].…”