Human antral damage induced by alcohol is potentiated by enprostil.

  title={Human antral damage induced by alcohol is potentiated by enprostil.},
  author={M. M. Cohen and R Yeung and H R Wang and L Clark},
  volume={99 1},
Enprostil, a synthetic analogue of prostaglandin E2, has been shown to protect the human gastroduodenal mucosa from aspirin injury. This study was designed to determine if enprostil protected against alcohol damage. A double-blind, randomized, cross-over study was performed on eight healthy adult men. After an overnight fast, a gastroscope was inserted and the antral mucosa was sprayed with a 10-mL test solution containing either enprostil (70 micrograms) or its vehicle (control). After 15… Expand
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Effects of Beer on the Gastric Mucosa as Determined by Endoscopy
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Circulatory mechanisms of gastric mucosal damage and protection.
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Comparison of oral sodium phosphate to polyethylene glycol-based solution for bowel preparation for colonoscopy in children.
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Protection against aspirin-induced antral and duodenal damage with enprostil. A double-blind endoscopic study.
The ability of enprostil, a synthetic analog of prostaglandin E2, given concurrently to prevent gastroduodenal injury was tested and it was found that the 7-micrograms dose protected only the antral mucosa, while the 70 micrograms b.i.d. afforded significant protection of both the antrals and duodenAL mucosa. Expand
Protective effect of enprostil against aspirin-induced gastroduodenal mucosal injury in man. Comparison with cimetidine and sucralfate.
The protective effect of enprostil was greatest in the antrum, the site of maximal mucosal injury, and Gastrointestinal side effects were reported in all groups, though abdominal pain and dyspepsia were noted more frequently in those taking enProstil. Expand
Preventing acetylsalicylic acid damage to human gastric mucosa by use of prostaglandin E2.
It is demonstrated that ASA damage to human gastric mucosa can be prevented entirely by concurrent administration of as little as 100 micrograms of PGE2, which supports the view that mucosal protection is a physiologic function of P GE2. Expand
Cytoprotection by a synthetic prostaglandin against ethanol-induced gastric mucosal damage. A double-blind endoscopic study in human subjects.
Misoprostol significantly prevented gastric mucosal injury with a mean endoscopic score of 1 +/- 1.7 when compared to placebo and to cimetidine, and may prove to be clinically very important and warrants further investigation. Expand
Reduction by enprostil of aspirin-induced blood loss from human gastric mucosa.
Enprostil reduced aspirin-induced mucosal blood loss but the mechanism is unclear, and the pH of both aspirated gastric juice and washings was significantly elevated, suggesting that an antisecretory dose had been used. Expand
Results provide the first clear indication that NSAID-induced ulcers are preventable, and Mild to moderate, self-limiting diarrhoea was the most frequently reported adverse effect attributed to misoprostol. Expand
Sucralfate protection of human gastric mucosa against acute ethanol injury.
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Antisecretory and serum gastrin lowering effect of enprostil in patients with duodenal ulcer disease.
This study suggests that, in addition to its cytoprotective effect, enprostil has potent antisecretory and antigastrin properties and is as effective as cimetidine 600 mg b.i.d. Expand
Enprostil and ranitidine in duodenal ulcer healing: double blind comparative trial.
The observed superiority of ranitidine 150 mg twice daily over enprostil 35 micrograms twice daily questions the clinical relevance of using so called "cytoprotection" as treatment for duodenal ulcer disease in the short term. Expand
Protective effect of prostaglandin E2 in the gastrointestinal tract during indomethacin treatment of rheumatic diseases
A protective effect on the gastrointestinal mucosa by oral prostaglandin E 2 has by the present study been demonstrated also in humans, and the finding may have clinical application, as gastrointestinal side effects and bleeding are common reasons for discontinuation of NSAID in patients with rheumatic diseases. Expand