Original communication| Volume 93, ISSUE 6, P786-791, June 1983

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Correlation of release and actions of cholecystokinin in dogs before and after vagotomy

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      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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