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Abstract
Pancreatic secretion of enzymes and gallbladder contraction in response to intestinal
stimulants are thought to be mediated through the vagus nerve and by means of release
of cholecystokinin (CCK). The effect of truncal vagotomy on the release of CCK, pancreatic
protein secretion, and gallbladder pressure (all stimulated by intraduodenal instillation
of oleate) was studied in five dogs. Each dog was prepared with chronic pancreatic
and gastric fistulas and catheter cholecystostomies. Simultaneous measurements were
made of plasma CCK (by radioimmunoassay), pancreatic protein secretion, and gallbladder
pressure (by perfused catheter technique) before and during intraduodenal administration
of oleate. Before truncal vagotomy, intraduodenal oleate caused increases in plasma
CCK (from 82 ± 6 to 208 ± 32 pg/ml), pancreatic protein secretion (from 83 ± 8 to
165 ± 15 mg/15 min), and gallbladder pressure (from 77 ± 2 to 27 ± 2 cm H2O) (all measured from basal state to 120 minutes). Truncal vagotomy caused a 45% decrease
in the output of pancreatic protein in response to oleate and completely abolished
the increase in gallbladder pressure, but it caused no change in release of CCK. The
correlations between plasma CCK and pancreatic protein secretion before truncal vagotomy
(r = 0.86) and after truncal vagotomy (r = 0.77) were highly significant. The correlation
between plasma CCK and gallbladder pressure was highly significant before (r = 0.91)
but not after (r = 0.42) truncal vagotomy. This study demonstrates that truncal vagotomy
inhibits pancreatic protein secretion and gallbladder pressure in response to fat
but does not interfere with release of CCK. The effects may be due to interruption
of vagus-mediated reflexes between the intestine and the pancreas and gallbladder.
The good correlation between plasma concentrations of CCK and both pancreatic protein
secretion and gallbladder pressure provides evidence that the radioimmunoassay measures
biologically active CCK.
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Article info
Publication history
Accepted:
September 22,
1982
Footnotes
☆Supported by National Institutes of Health grant AM 15241 and Moody Foundation grant 81-57.
Identification
Copyright
© 1983 Published by Elsevier Inc.
