Protection of the gastroduodenal mucosa by prostaglandins.
Like other nucleated cell populations in the body, the cells of the gastroduodenal mucosa are capable to metabolise arachidonic acid into prostaglandins, with prostaglandin E2 as the probable major metabolite. The production increases on demand and can be followed in the gastric lumen, where the output of prostaglandin E2 increases two to fourfold after exposure of the mucosa to hydrochloric acid. Exogenous prostaglandins, in particular of the E series, stimulate several identified mucosal defense factors in the upper gastrointestinal tract. Prostaglandins of the E series stimulate the transport of bicarbonate and the production and release of mucus glycoproteins from the gastroduodenal mucosa. They have trophic effects on gastrointestinal epithelia by increasing the survival time of mucosal cells and have cytoprotective properties. In addition, E2 prostaglandins suppress the gastric acid secretion and accelerate peptic ulcer healing. Non steroidal antiinflammatory drugs, which block the biosynthesis of prostaglandins, suppress the bicarbonate secretion, the production of mucus glycoproteins and cytoprotective properties. They interfere with the inhibitory feedback regulation of the gastric acid secretion and are ulcerogenic in experimental and clinical situations. These actions of PG biosynthesis blockers provide indirect information on the importance of local prostaglandin formation for maintenance of gastrointestinal mucosal integrity. It is hypothesised that biosynthesis of prostaglandins in the gastroduodenal mucosa is of importance and may be a key event in triggering the different components of the mucosal defense.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects; D000897:Anti-Ulcer Agents / Q000494:pharmacology; D001639:Bicarbonates / Q000378:metabolism; D002470:Cell Survival; D000431:Ethanol / Q000633:toxicity; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced; D006801:Humans; D007413:Intestinal Mucosa / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010437:Peptic Ulcer / Q000139:chemically induced; D011448:Prostaglandin Antagonists / Q000009:adverse effects; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats
D000893:Anti-Inflammatory Agents; D000897:Anti-Ulcer Agents; D001639:Bicarbonates; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011458:Prostaglandins E; D000431:Ethanol