title: Acid instillation increases gastric luminal prostaglandin E2 output in man.
abstract: The capacity of the gastroduodenal mucosa to maintain integrity when exposed to acid and pepsin may require formation of endogenous prostaglandins (PG). The gastric mucosa is capable of PG biosynthesis, and PGE2 is present in the gastric contents of man. The purpose of this study was to examine if acidification of the human stomach affects the output of PGE2. Gastric perfusion was made with 150 mM HCl in seven healthy subjects pretreated with a histamine-2-receptor blocker (ranitidine). Gastric luminal PGE2 was measured by gas chromatography-mass spectrometry. Basal output of PGE2 was 1.42 +/- 0.24 pmol/min (mean + SEM), which increased to 5.37 +/- 0.91 pmol/min (p less than 0.02) during acid perfusion. Gastric acidification did not cause mucosal damage as judged by luminal DNA. We conclude that PGE2 is synthesized in the gastric mucosa even during nearly complete inhibition of parietal cell secretion. Luminal acid, a likely physiological stimulator of mucosal defense, induces a fivefold increase in PGE2 output from the intact mucosa.
mesh_terms: D000328:Adult; D004247:DNA / Q000378:metabolism; D015232:Dinoprostone; D004386:Duodenum; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D011458:Prostaglandins E / Q000378:metabolism*; D011899:Ranitidine / Q000494:pharmacology
chemical_list: D011458:Prostaglandins E; D011899:Ranitidine; D004247:DNA; D015232:Dinoprostone