Possible Role of Endogenous Prostaglandins Against Ethanol Injury in Rat Stomach

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Abstract
Exposure of the gastric mucosa for 3 min to 30% intragasric ethanol induced mucosal injury that appeared dark red n anesthetized rats. Microscopic observation of the microvasculature in the injured area after exsanguination of rats and living rats confirmed that there was congestion of the blood flow in the collecting venules and capillaries. Hemor-chage was observed about 30 min after application of ethanol. Monastral blue dye was deposited along the postcapilary venules only at the border of the congestion area. A selective 5-lipoxygenase inhibitor, AA-861, inhibited the gastric lesion, and immunoreactive leukotriene C4 (LTC4) was detected in the gastric wall. Previous exposure of the gastric mucosa to 1.0 M NaCl solution inhibited the ethanol-induced mucosal injury markedly. NaCl solutions 0.5–1.0 M) also suppressed the electrical activity of smooth muscle and the suppression was released by indomethacin. Having observed that PGE2 generation in the stomach was induced dose-dependently by intragastric NaCl solutions (0.5–1.0 M), we propose the hypothesis that Peptide LTs released by intragastric ethanol constrict the Collecting venules or lamina muscularis mucosae and induce congestion of these venules. whereas the PGE2 released by intragastric NaCl solution releases the congestion Of the collecting venules directly or through suppression of contraction of the lamina muscularis.

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