Abstract
Omeprazole, a substituted benzimidazole, inhibits basal and stimulated gastric acid secretion in animals and humans in a dose dependent fashion, for long periods after oral administration. This antisecretory effect is probably due to non-competitive inhibition of the H+K+ATPase proton pump which has been identified in the secretory membrane of the parietal cell. Preliminary data from animal experiments have indicated that oral omeprazole, 400 μmol/kg, also delays gastrin emptying but intravenous omeprazole, 80 μmol/kg, does not, As the plasma concentrations of omeprazole following administration by both routes were similar, a local rather than a systemic effect was suggested. Therefore, in this study the effect has been evaluated of a single oral dose of omeprazole, 90 mg, given as a buffered, uncoated granulate, on gastric emptying of a mixed liquid and solid meal in patients with duodenal ulcer disease.
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