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 multip le factors enhancing pancreatic exocrine secretion using a rat model of pan creatic bile duct (ligatian (PBDL)-induced pancreatitis, Under fasting and non-fasting conditions, a PBDL group, a second group treated by hepatic bil e 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 th e 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. Di version of pancreatic and/or bile juice in these groups resulted in no incr ease of S-amylase activity: Truncal vagotomy or injection of an anticholine rgic drug or a cholecystokinin (CCK)(1)-receptor antagonist inhibited pancr eatic exocrine secretion and S-amylase activity in the non-fasting PBDL gro up 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 inf low of bile and pancreatic juice commonly enhance pancreatic exocrine secre tion, acting synergistically as aggravating factors in pancreatitis. CCK: a nd the vagus nerve system appears to be involved in enhancing pancreatic ex ocrine secretion with diet stimulation as an aggravating factor.