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Previous Volume 293:371-375 August 21, 1975 Number 8 Next

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Abstract

Cimetidine, a non-thiourea-containing H2-receptor antagonist, was studied in seven patients with duodenal ulcer. Oral doses of 100, 200, and 300 mg were tested. Each dose significantly inhibited basal and meal-stimulated secretion. After 300 mg, basal acid secretion was essentially zero for at least five hours. The meal-stimulated three-hour acid output after the 300-mg dose was reduced by 67%. Cimetidine, 300 mg, decreased meal-stimulated acid secretion significantly more than an optimal effective dose of propantheline bromide (P less than 0.05). Inhibition of meal-stimualted gastric acid secretion showed a significant relation to peak blood cimetidine concentration (r is equal to 0.76, P less than 0.01). Cimetidine did not affect meal-stimulated gastrin release. No toxicity was observed after serial doses given during these tests. Cimetidine may be useful in treatment of acid-peptic diseases provided no important toxicity appears on chronic testing.

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• KISLOFF, B. (1980). Cimetidine-Resistant Gastric Acid Secretion in Humans. ANN INTERN MED 92: 791-793 [Abstract]  
• SILVER, B. A., BELL, W. R. (1979). Cimetidine Potentiation of the Hypoprothrombinemic Effect of Warfarin. ANN INTERN MED 90: 348-349 [Abstract]  
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• MCCARTHY, D. M., OLINGER, E. J., MAY, R. J., LONG, B. W., GARDNER, J. D. (1977). H2-Histamine Receptor Blocking Agents in the Zollinger-Ellison Syndrome: Experience in Seven Cases and Implications for Long-Term Therapy. ANN INTERN MED 87: 668-675 [Abstract]  
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