Abstract There is an increased incidence of gallstones after truncal vagotomy but the mechanism is unknown. Our aim was to study the early effects of vagotomy on fasting and postprandial gallbladder motility. A chronic model was constructed in 10 dogs to correlate gallbladder motility and emptying w
Effects of somatostatin and loxiglumide on gallbladder motility
β Scribed by R. J. Lieverse; M. C. W. Jebbink; A. A. M. Masclee; C. B. H. W. Lamers; J. B. M. J. Jansen; L. C. Rovati
- Publisher
- Springer
- Year
- 1995
- Tongue
- English
- Weight
- 379 KB
- Volume
- 47
- Category
- Article
- ISSN
- 0031-6970
No coin nor oath required. For personal study only.
β¦ Synopsis
Cholecystokinin (CCK) is the major hormonal stimulus of gallbladder contraction. Both somatostatin and CCK-A receptor antagonists inhibit stimulation of the gallbladder by CCK. The aim of this study was to compare the effect of somatostatin and the CCK-A receptor antagonist loxiglumide (CR 1505) on gallbladder volume at baseline and after feeding.
In random order nine healthy subjects received somatostatin (IV loading dose 125 ~g, followed by IV infusion of 125 9g h-l), loxiglumide (10 rag. kg -1 β’ h -1) and control saline. Gallbladder volumes and plasma CCK levels were measured basally and during stimulation by an intraduodenal infusion of fat using, respectively, ultrasound and a sensitive and specific radioimmunoassay.
Mean basal gallbladder volume was similar prior to the saline control (28.5 ml), loxiglumide (28.7 ml) and somatostatin (23.4 ml) experiments. In the control experiment, intraduodenal fat led to a significant increase in plasma CCK from 2.6 to 4.8 pmol. 1-1, accompanied by contraction of the gallbladder to 2.0 ml. Loxiglumide induced dilatation of the gallbladder to 40 ml and prevented the any contraction in response to intraduodenal fat. During the somatostatin infusion, gallbladder volume remained the same both basally and during fat stimulation. The plasma CCK response to intraduodenal fat was exaggerated by loxiglumide and was abolished by somatostatin.
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