Abstract
Misoprostol, a synthetic derivative of prostaglandin E1, was tested and shown to be an effective gastric antisecretory agent against histamine-, pentagastrin-, and meal-stimulated acid secretion in dogs. Misoprostol reduced the volume of acid secretion as well as the hydrogen ion concentration. Misoprostol did not reduce gastric mucosal blood flow, nor did it alter meal-stimulated serum gastrin levels. Misoprostol inhibited acid secretion in histamine-stimulated isolated gastric glands indicating a direct antisecretory effect on parietal cells. The potency of misoprostol was greatest when administered in direct contact with the gastric mucosa indicating local absorption and action. Misoprostol strengthened the gastric mucosal barrier as shown by the attenuation of aspirin-induced lowering of transmucosal electrical potential differences. Misoprostol protected the gastric mucosa of rats subjected to ethanol-, taurocholate-, pyloric ligation-, stress- and indomethacin-induced damage. Misoprostol also protected against indomethacin-induced intestinal lesions in rats and reduced duodenal ulcer formation in guinea-pigs and cats. The doses of misoprostol required to protect against gastric damage were about one-tenth of those required to inhibit acid secretion. The results of these and other studies indicate that misoprostol is a safe agent with unique properties that should provide a new approach for treatment of ulcer diseases of the gastrointestinal tract.
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Bauer, R.F. Misoprostol preclinical pharmacology. Digest Dis Sci 30 (Suppl 11), 118S–125S (1985). https://doi.org/10.1007/BF01309396
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DOI: https://doi.org/10.1007/BF01309396