Rj. Lieverse et al., EFFECTS OF SOMATOSTATIN AND LOXIGLUMIDE ON GALLBLADDER MOTILITY, European Journal of Clinical Pharmacology, 47(6), 1995, pp. 489-492
Cholecystokinin (CCK) is the major hormonal stimulus of gallbladder co
ntraction. Both somatostatin and CCK-A receptor antagonists inhibit st
imulation of the gallbladder by CCK. The aim of this study was to comp
are the effect of somatostatin and the CCK-A receptor antagonist loxig
lumide (CR 1505) on gallbladder volume at baseline and after feeding.
In random order nine healthy subjects received somatostatin (IV loadin
g dose 125 mu g, followed by IV infusion of 125 mu g h(-1)), loxiglumi
de (10 mg . kg(-1) . h(-1)) and control saline. Gallbladder volumes an
d plasma CCK levels were measured basally and during stimulation by an
intraduodenal infusion of fat using, respectively, ultrasound and a s
ensitive and specific radioimmunoassay. Mean basal gallbladder volume
was similar prior to the saline control (28.5 ml), loxiglumide (28.7 m
l) 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 . l(-1), accompanied by contraction of the gallbladder to
2.0 ml. Loxiglumide induced dilatation of the gallbladder to 40 ml an
d prevented the any contraction in response to intraduodenal fat. Duri
ng the somatostatin infusion, gallbladder volume remained the same bot
h basally and during fat stimulation. The plasma CCK response to intra
duodenal fat was exaggerated by loxiglumide and was abolished by somat
ostatin. We conclude that there are major differences between the effe
cts of loxiglumide and somatostatin on gallbladder motility. Loxiglumi
de dilates the gallbladder, while somatostatin prevents its contractio
n during fat stimulation.