AJP - Gastrointestinal and Liver Physiology, Vol 262, Issue 5 909-G914, Copyright © 1992 by American Physiological Society
Effect of octreotide on sphincter of Oddi and gallbladder motility in prairie dogs
S. A. Ahrendt, G. M. Ahrendt, K. D. Lillemoe and H. A. Pitt
Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Somatostatin and its synthetic analogue, octreotide, inhibit gallbladder
emptying and cause gallstones. Whether octreotide-induced alterations in
sphincter of Oddi motility contribute to this process is unknown. We,
therefore, examined the effect of octreotide on fasting and
protein-stimulated sphincter of Oddi motility. In 25 anesthetized prairie
dogs, sphincter of Oddi motility and gallbladder pressure were monitored
during the intravenous administration of octreotide, cholecystokinin (CCK)
octapeptide, atropine, the intraduodenal administration of casein, and
combinations of these agents. Intravenous octreotide decreased fasting
sphincter of Oddi motility index both with (59 +/- 19 vs. 84 +/- 28, P less
than 0.05) and without (137 +/- 31 vs. 227 +/- 42, P less than 0.05) prior
cholinergic blockade with atropine. Octreotide also prevented the increases
in sphincter of Oddi motility and gallbladder pressure seen with
intraduodenal casein. Exogenous CCK increased sphincter of Oddi motility
index and gallbladder pressure despite the simultaneous administration of
octreotide alone (357 +/- 109 vs. 137 +/- 31, P less than 0.07, and 11.2
+/- 1.0 mmHg vs. 9.6 +/- 0.6 mmHg, P less than 0.05) or the combination of
octreotide and atropine (317 +/- 69 vs. 59 +/- 19, P less than 0.05, and
10.1 +/- 1.6 mmHg vs. 8.5 +/- 1.4 mmHg, P less than 0.05). We conclude that
both a cholinergic and an octreotide-sensitive noncholinergic pathway
stimulate fasting sphincter of Oddi motility in the prairie dog.
