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The role of cholecystokinin and the cholinergic system in intravenous amino acid-induced gallbladder emptying.
Eur J Gastroenterol Hepatol. 1997 Dec; 9(12):1227-31.EJ

Abstract

BACKGROUND

Recent studies have demonstrated that separate intravenous infusion of amino acids (IVAA) at high doses induces gallbladder emptying. However, little is known about the mechanisms mediating IVAA-induced gallbladder contraction.

OBJECTIVE AND METHODS

To investigate whether the effect of IVAA on gallbladder motility is mediated by the cholinergic system and/or cholecystokinin (CCK), the major hormonal stimulus for gallbladder contraction. Six healthy male volunteers were studied in random order on five occasions using: (a) IVAA, (b) loxiglumide (CR 1505, a selective CCK-A receptor antagonist), (c) IVAA plus loxiglumide, (d) atropine and (e) IVAA plus atropine. Gallbladder volumes (ultrasonography) and plasma CCK levels (radioimmunoassay) were determined every 15 min for 60 min before and for 120 min during intravenous infusion of amino acids (Vamin 18EF; 250 mg protein/kg/h) and/or loxiglumide (10 mg/kg/h) and/or atropine (0.005 mg/kg/h).

RESULTS

IVAA significantly (P < 0.05) reduced gallbladder volume from 32 +/- 5 ml to 17 +/- 2 ml but induced only a small and transient increase in plasma CCK levels. Loxiglumide given alone significantly (P < 0.05) increased fasting gallbladder volume to 190% of the basal value. IVAA-induced gallbladder emptying was completely abolished by loxiglumide. Maximal gallbladder relaxation during IVAA plus loxiglumide was not significantly different compared to loxiglumide given alone. Concomitant administration of atropine also significantly (P < 0.05) inhibited IVAA-induced gallbladder emptying.

CONCLUSION

In healthy volunteers intravenous infusion of high doses of amino acids results in a significant gallbladder contraction, which is inhibited by CCK-A receptor blockade and by atropine.

Authors+Show Affiliations

Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

9471030

Citation

Gielkens, H A., et al. "The Role of Cholecystokinin and the Cholinergic System in Intravenous Amino Acid-induced Gallbladder Emptying." European Journal of Gastroenterology & Hepatology, vol. 9, no. 12, 1997, pp. 1227-31.
Gielkens HA, de Boer SY, Lam WF, et al. The role of cholecystokinin and the cholinergic system in intravenous amino acid-induced gallbladder emptying. Eur J Gastroenterol Hepatol. 1997;9(12):1227-31.
Gielkens, H. A., de Boer, S. Y., Lam, W. F., Rovati, L. C., Lamers, C. B., & Masclee, A. A. (1997). The role of cholecystokinin and the cholinergic system in intravenous amino acid-induced gallbladder emptying. European Journal of Gastroenterology & Hepatology, 9(12), 1227-31.
Gielkens HA, et al. The Role of Cholecystokinin and the Cholinergic System in Intravenous Amino Acid-induced Gallbladder Emptying. Eur J Gastroenterol Hepatol. 1997;9(12):1227-31. PubMed PMID: 9471030.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of cholecystokinin and the cholinergic system in intravenous amino acid-induced gallbladder emptying. AU - Gielkens,H A, AU - de Boer,S Y, AU - Lam,W F, AU - Rovati,L C, AU - Lamers,C B, AU - Masclee,A A, PY - 1998/2/21/pubmed PY - 1998/2/21/medline PY - 1998/2/21/entrez SP - 1227 EP - 31 JF - European journal of gastroenterology & hepatology JO - Eur J Gastroenterol Hepatol VL - 9 IS - 12 N2 - BACKGROUND: Recent studies have demonstrated that separate intravenous infusion of amino acids (IVAA) at high doses induces gallbladder emptying. However, little is known about the mechanisms mediating IVAA-induced gallbladder contraction. OBJECTIVE AND METHODS: To investigate whether the effect of IVAA on gallbladder motility is mediated by the cholinergic system and/or cholecystokinin (CCK), the major hormonal stimulus for gallbladder contraction. Six healthy male volunteers were studied in random order on five occasions using: (a) IVAA, (b) loxiglumide (CR 1505, a selective CCK-A receptor antagonist), (c) IVAA plus loxiglumide, (d) atropine and (e) IVAA plus atropine. Gallbladder volumes (ultrasonography) and plasma CCK levels (radioimmunoassay) were determined every 15 min for 60 min before and for 120 min during intravenous infusion of amino acids (Vamin 18EF; 250 mg protein/kg/h) and/or loxiglumide (10 mg/kg/h) and/or atropine (0.005 mg/kg/h). RESULTS: IVAA significantly (P < 0.05) reduced gallbladder volume from 32 +/- 5 ml to 17 +/- 2 ml but induced only a small and transient increase in plasma CCK levels. Loxiglumide given alone significantly (P < 0.05) increased fasting gallbladder volume to 190% of the basal value. IVAA-induced gallbladder emptying was completely abolished by loxiglumide. Maximal gallbladder relaxation during IVAA plus loxiglumide was not significantly different compared to loxiglumide given alone. Concomitant administration of atropine also significantly (P < 0.05) inhibited IVAA-induced gallbladder emptying. CONCLUSION: In healthy volunteers intravenous infusion of high doses of amino acids results in a significant gallbladder contraction, which is inhibited by CCK-A receptor blockade and by atropine. SN - 0954-691X UR - https://www.unboundmedicine.com/medline/citation/9471030/The_role_of_cholecystokinin_and_the_cholinergic_system_in_intravenous_amino_acid_induced_gallbladder_emptying_ DB - PRIME DP - Unbound Medicine ER -