K. Yoshinaga et al., Diet stimulation as a synergistic factor of aggravation in a pancreatic bile duct ligation-induced rat pancreatitis model, BIOL PHAR B, 23(11), 2000, pp. 1318-1322
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.