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Inhibition of pancreaticobiliary secretion by loperamide in humans
Author(s) -
Thimister P W L,
Hopman W P,
van Roermund R F C,
Willems H L,
Rosenbusch G,
Woestenborghs R,
Jansen J B
Publication year - 1997
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510260201
Subject(s) - loperamide , medicine , cholecystokinin , endocrinology , postprandial , motilin , gallbladder , basal (medicine) , gastrointestinal hormone , chemistry , peptide hormone , receptor , diarrhea , insulin
Abstract Loperamide, a peripherally acting opiate receptor agonist with antidiarrheal action, inhibits ileal and colonic motor function. It was determined whether loperamide also affects gallbladder emptying and pancreatic enzyme secretion in humans. Plasma cholecystokinin (radioimmunoassay), gallbladder volume (ultrasonography), and intraduodenal bilirubin and amylase output (spot sampling) were measured at regular intervals before and during intraduodenal perfusion of an amino acid meal in 8 healthy subjects: once without and once with pretreatment of 8 mg loperamide, ingested 13 and 4 hours before the start of the meal. Loperamide decreased basal amylase output from 3.2 ± 0.5 to 1.0 ± 0.5 kU/h (P < .005) and abolished basal bilirubin output (21 ± 5 vs. 0 ± 0 micromol/h; P < .005) into the duodenum. Loperamide increased basal gallbladder volume from 28 ± 4 to 39 ± 4 mL (P < .0001) but was without effect on basal plasma cholecystokinin (2.7 ± 0.3 vs. 3.0 ± 0.3 pmol/L). During the amino acid meal, pretreatment with loperamide inhibited amylase output from 5.1 ± 0.8 to 1.6 ± 0.4 kU/h (P < .001), bilirubin output from 39 ± 6 to 18 ± 6 micromol/h (P < .0005) and gallbladder contraction from 47% ± 3% to 26% ± 6% (P < .05), whereas loperamide enhanced amino acid‐stimulated plasma cholecystokinin from 4.5 ± 1.6 to 7.6 ± 1.0 pmol/L (P < .05). It is concluded that loperamide inhibits basal and amino acid‐stimulated gallbladder motility and intraduodenal output of bilirubin and amylase, despite an enhanced postprandial cholecystokinin release.