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Omeprazole promotes proximal duodenal mucosal bicarbonate secretion in humans.
Gut. 1996 Jan; 38(1):6-10.Gut

Abstract

The proton pump inhibitor, omeprazole, surprisingly resulted in higher rates of proximal duodenal mucosal bicarbonate secretion than previously reported using an H2 receptor antagonist for gastric acid inhibition. Gastroduodenal perfusions were performed in healthy volunteers to evaluate whether this incidental finding is explained by more potent gastric acid inhibition by omeprazole or might be caused by the different mode of drug action. Basal and stimulated gastric and duodenal bicarbonate secretion rates were measured in the same subjects in control experiments (n = 17) and after pretreatment with high dose omeprazole (n = 17) and ranitidine (n = 9), respectively, by use of a technique permitting simultaneous measurements. Concentrations of bicarbonate were measured in the respective effluents by the method of back titration. Both omeprazole and ranitidine completely inhibited gastric acid secretion (pH 6.9 v 6.8; p > 0.05). Omeprazole caused higher rates of basal (mean (SEM)) (597 (48) v 351 (39) mumol/h; p < 0.02) and vagally stimulated (834 (72) v 474 (66) mumol/h; p < 0.02), but not acid stimulated (3351 (678) v 2550 (456) mumol/h; p > 0.05) duodenal bicarbonate secretion compared with control experiments. Also the combination of omeprazole and ranitidine increased (p = 0.05) duodenal bicarbonate secretion, while ranitidine alone caused no change in either basal or stimulated secretion. In the stomach basal as well as vagally stimulated bicarbonate secretion was independent of the means of acid inhibition. These results show that the proton pump inhibitor, omeprazole, promotes proximal duodenal mucosal bicarbonate secretion apparently independent of its gastric acid inhibitory effect. The mechanism of action remains speculative.

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Authors+Show Affiliations

Mertz-Nielsen A
Department of Medical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Denmark.
Hillingsø J
No affiliation info available
Bukhave K
No affiliation info available
Rask-Madsen J
No affiliation info available

MeSH

AdultAnti-Ulcer AgentsBicarbonatesDuodenumFemaleHumansIntestinal SecretionsMaleMiddle AgedOmeprazoleRanitidine

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8566861

Citation

Mertz-Nielsen, A, et al. "Omeprazole Promotes Proximal Duodenal Mucosal Bicarbonate Secretion in Humans." Gut, vol. 38, no. 1, 1996, pp. 6-10.
Mertz-Nielsen A, Hillingsø J, Bukhave K, et al. Omeprazole promotes proximal duodenal mucosal bicarbonate secretion in humans. Gut. 1996;38(1):6-10.
Mertz-Nielsen, A., Hillingsø, J., Bukhave, K., & Rask-Madsen, J. (1996). Omeprazole promotes proximal duodenal mucosal bicarbonate secretion in humans. Gut, 38(1), 6-10.
Mertz-Nielsen A, et al. Omeprazole Promotes Proximal Duodenal Mucosal Bicarbonate Secretion in Humans. Gut. 1996;38(1):6-10. PubMed PMID: 8566861.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Omeprazole promotes proximal duodenal mucosal bicarbonate secretion in humans. AU - Mertz-Nielsen,A, AU - Hillingsø,J, AU - Bukhave,K, AU - Rask-Madsen,J, PY - 1996/1/1/pubmed PY - 1996/1/1/medline PY - 1996/1/1/entrez SP - 6 EP - 10 JF - Gut JO - Gut VL - 38 IS - 1 N2 - The proton pump inhibitor, omeprazole, surprisingly resulted in higher rates of proximal duodenal mucosal bicarbonate secretion than previously reported using an H2 receptor antagonist for gastric acid inhibition. Gastroduodenal perfusions were performed in healthy volunteers to evaluate whether this incidental finding is explained by more potent gastric acid inhibition by omeprazole or might be caused by the different mode of drug action. Basal and stimulated gastric and duodenal bicarbonate secretion rates were measured in the same subjects in control experiments (n = 17) and after pretreatment with high dose omeprazole (n = 17) and ranitidine (n = 9), respectively, by use of a technique permitting simultaneous measurements. Concentrations of bicarbonate were measured in the respective effluents by the method of back titration. Both omeprazole and ranitidine completely inhibited gastric acid secretion (pH 6.9 v 6.8; p > 0.05). Omeprazole caused higher rates of basal (mean (SEM)) (597 (48) v 351 (39) mumol/h; p < 0.02) and vagally stimulated (834 (72) v 474 (66) mumol/h; p < 0.02), but not acid stimulated (3351 (678) v 2550 (456) mumol/h; p > 0.05) duodenal bicarbonate secretion compared with control experiments. Also the combination of omeprazole and ranitidine increased (p = 0.05) duodenal bicarbonate secretion, while ranitidine alone caused no change in either basal or stimulated secretion. In the stomach basal as well as vagally stimulated bicarbonate secretion was independent of the means of acid inhibition. These results show that the proton pump inhibitor, omeprazole, promotes proximal duodenal mucosal bicarbonate secretion apparently independent of its gastric acid inhibitory effect. The mechanism of action remains speculative. SN - 0017-5749 UR - https://www.unboundmedicine.com/medline/citation/8566861/Omeprazole_promotes_proximal_duodenal_mucosal_bicarbonate_secretion_in_humans_ L2 - https://gut.bmj.com/lookup/pmidlookup?view=long&amp;pmid=8566861 DB - PRIME DP - Unbound Medicine ER -