DUCTAL AND VASCULAR FACTORS IN ETIOLOGY OF EXPERIMENTALLY INDUCED PANCREATIC FIBROSIS AND FAT REPLACEMENT IN DOGS

Abstract

To demonstrate the progress of pathogenesis of pancreatic fibrosis and fat replacement, ductal and vascular obstructions were imposed on 5 groups of mongrel dogs.
When the pancreatic duct alone was obstructed in the first group of 10 dogs, mild acute pancreatitis, including pancreatic parenchymal edema associated with inflammatory cells, was found during the early stage. During the late stage, however, interlobular and intralobular fibrosis (also called pancreatic fibrosis) were seen.
In a second group of 14 dogs receiving obstructions to both the pancreatic duct and major pancreatic arteries, acute necrotizing pancreatitis, including pancreatic parenchymal necrosis and interlobular fibrosis, was apparent in the early stage. However, pancreatic fibrosis increased and sporadic or collected pancreatic fat replacement was seen in the later stage.
A third group of 10 dogs receiving obstructions to both the pancreatic duct and major pancreatic veins, and a fourth group of 7 dogs receiving obstructions to both the pancreatic duct and pancreatic lymph channels showed pathologic findings similar to the first group.
In a fifth group of 2 dogs with obstructions to the major pancreatic arteries imposed for 1 week after obstruction of the pancreatic ducts for 8 weeks, severe pancreatic fibrosis and fat replacement, similar to chronic pancreatitis in humans, were observed.
The foregoing results indicate that (1) pancreatic ischemia is an important factor influencing the induction of pancreatic fibrosis and fat replacement, and (2) pancreatic fat replacement is caused by chronic pancreatic ischemia.