Effects of lorglumide on gastrin- and peptone-stimulated gastric acid secretion in rats
This study in rats demonstrates that gastric acid secretion stimulated by infusion of gastrin 17-l yielding plasma concentrations in the physiological range is almost abolished by the cholecystokinin-receptor antagonist lorglumide. Furthermore, lorglumide also inhibited intragastric peptone stimulat...
Gespeichert in:
Veröffentlicht in: | Life sciences (1973) 1990, Vol.47 (26), p.2459-2464 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | This study in rats demonstrates that gastric acid secretion stimulated by infusion of gastrin 17-l yielding plasma concentrations in the physiological range is almost abolished by the cholecystokinin-receptor antagonist lorglumide. Furthermore, lorglumide also inhibited intragastric peptone stimulated gastric acid secretion by 43%. When compared to peptone stimulation with a saline background infusion, lorglumide infusion inhibited peptone stimulated gastric acid secretion only significantly in the late (20 to 30 minutes) part of stimulation, while the initial part (0 to 10 and 10 to 20 minutes) was not significantly inhibited by lorglumide. Both peptone stimulation and gastrin infusion significantly augmented serum gastrin concentrations, which were not significantly influenced by lorglumide. The serum gastrin concentrations achieved during gastrin infusion were higher than during peptone stimulation, however the differences were not statistically significant. It is concluded that lorglumide abolishes gastrin stimulated gastric acid secretion in rats, but only partly (43%) inhibits peptone-meal stimulated gastric acid secretion. In contrast to the gastrin infusion experiments, where lorglumide abolishes acid secretion during the entire study period, the compound inhibits gastric acid secretion more effectively towards the end of peptone stimulation than in the beginning. |
---|---|
ISSN: | 0024-3205 1879-0631 |
DOI: | 10.1016/0024-3205(90)90491-9 |