Diet stimulation as a synergistic factor of aggravation in a pancreatic bile duct ligation-induced rat pancreatitis model.

We evaluated the association between aggravation of pancreatitis and multiple factors enhancing pancreatic exocrine secretion using a rat model of pancreatic bile duct ligation (PBDL)-induced pancreatitis. Under fasting and non-fasting conditions, a PBDL group, a second group treated by hepatic bile duct ligation (BDL) and a third group treated by pancreatic duct ligation (PDL) were compared in terms of serum amylase (S-amylase) activity. The S-amylase activity in the PBDL group was higher than in the sham group. In the PDL group, the increase in S-amylase activity was lower than in the PBDL group. In the BDL group, no increase in S-amylase activity was observed. Diversion of pancreatic and/or bile juice in these groups resulted in no increase of S-amylase activity. Truncal vagotomy or injection of an anticholinergic drug or a cholecystokinin (CCK)1-receptor antagonist inhibited pancreatic exocrine secretion and S-amylase activity in the non-fasting PBDL group but not in the fasting PBDL group. These results suggest that retention of pancreatic juice in the pancreatic duct is necessary for the increase of S-amylase activity, and that dietary stimulation and impaired duodenal inflow of bile and pancreatic juice commonly enhance pancreatic exocrine secretion, acting synergistically as aggravating factors in pancreatitis. CCK and the vagus nerve system appears to be involved in enhancing pancreatic exocrine secretion with diet stimulation as an aggravating factor.