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Misoprostol inhibits gastric mucosal release of endogenous prostaglandin E and thromboxane B in healthy volunteers

Gut, ISSN: 0017-5749, Vol: 36, Issue: 4, Page: 511-515
1995
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Article Description

Prostaglandin analogues of the E-series theoretically offer the ideal antiulcer drugs. Peptic ulcer healing with prostaglandin analogues is, however, no better than would be predicted from their ability to inhibit gastric acid secretion and they are less effective than histamine H receptor antagonists in preventing ulcer relapse. It could be that prostaglandin analogues inhibit gastric mucosal synthesis or release of endogenous eicosanoids, thereby abrogating their own effects. This study, therefore, examined how a single therapeutic dose (200 μg) of misoprostol, a synthetic analogue of prostaglandin E, influences gastric mucosal release of endogenous prostaglandin E (PGE), thromboxane B (TXB), and chemotactic leukotriene B (LTB) during basal conditions and in response to gastric luminal acidification (0.1 M HCl; 5 ml/min for 10 minutes). Nine healthy volunteers were studied in a single blind, cross over design. In each subject misoprostol or placebo was instilled in randomised order into the stomach, which was subsequently perfused with isotonic mannitol. Misoprostol significantly decreased basal as well as acid stimulated output of PGE and TXB, without affecting output of LTB. These data show that misoprostol inhibits gastric mucosal synthesis of prostanoids. Decreased concentrations, or even a changed profile, of native eicosanoids modulating the release of inflammatory mediators from immune cells might explain why prostaglandin analogues have a comparatively poor clinical performance in ulcer healing and prevention.

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