Exocrine function of the pancreas in obstructive jaundice was examined
using dogs. Jaundice induced by choledochal ligation over 3 weeks sho
wed pancreatic hypersecretion in response to cholecystokinin octapepti
de (CCK-8) stimulation. To clarify the mechanism of pancreatic hyperse
cretion in obstructive jaundice, three experiments were undertaken. In
a perfusion experiment performed on isolated pancreas, hypersecretion
in obstructive jaundice was observed in response to CCK-8 stimulation
. An incubation experiment showed an increase in secretion in response
to CCK-8 stimulation in a dose-dependent manner, producing a greater
increase in dogs with obstructive jaundice than in controls, despite t
he fact that basal secretion in both groups was the same. This would s
uggest that at least one of the mechanisms of pancreatic hypersecretio
n in obstructive jaundice may be related to the degree of sensitivity
of acinar cells to CCK-8. In morphological observation of acinar cells
by electron microscopy, the average number of zymogen granules and to
tal granular area per unit of cytoplasm in both groups before and afte
r stimulation with CCK-8 were compared. There was no difference betwee
n the groups before stimulation. Following stimulation, values for the
control group decreased but appeared to increase in the jaundiced pan
creas. These results strongly suggest that pancreatic acinar cells in
obstructive jaundice may retain their secretory potential after stimul
ation for 60 min, though the potential in nonjaundiced pancreatic acin
ar cells may decrease after stimulation.