Effect of prostaglandin synthesis inhibitors on neurotensin and sodium salicylate-induced gastric cytoprotection in rats.
Sodium salicylate (SA) has been reported to inhibit the formation of gastric ulcerations induced by aspirin, indomethacin, and absolute ethanol. In this study, SA dose-dependently inhibited gastric ulcers induced by three hours of cold-restraint stress (CRS); SA-induced cytoprotection was prevented by both acetylsalicylic acid (aspirin) and indomethacin pretreatment. Neurotensin (NT), which has previously been demonstrated to prevent the development of CRS-induced gastric ulcerations after intracisternal administration, was found to be ineffective in animals pre-treated with aspirin, and with indomethacin, as previously described. These data suggest that in the CRS model both NT- and SA-induced gastric cytoprotection require a functionally intact gastrointestinal prostaglandin synthetic pathway.
D000818:Animals; D001241:Aspirin; D003080:Cold Temperature; D000431:Ethanol; D006801:Humans; D007213:Indomethacin; D008297:Male; D009496:Neurotensin / Q000494:pharmacology*; D011448:Prostaglandin Antagonists; D051381:Rats; D011919:Rats, Inbred Strains; D012149:Restraint, Physical; D012980:Sodium Salicylate / Q000494:pharmacology*; D013276:Stomach Ulcer / Q000139:chemically induced / Q000209:etiology / Q000517:prevention & control*; D013315:Stress, Psychological / Q000503:physiopathology
D011448:Prostaglandin Antagonists; D009496:Neurotensin; D000431:Ethanol; D001241:Aspirin; D012980:Sodium Salicylate; D007213:Indomethacin