Prevention of ethanol and aspirin-induced gastric mucosal lesions by paracetamol and salicylate in rats: role of endogenous prostaglandins.
Paracetamol or sodium salicylate given intragastrically 30 minutes before the administration of absolute ethanol or acidified aspirin dose-dependently reduced the formation of mucosal lesions. The generation of gastric mucosal prostaglandin-like activity increased with ethanol and was completely suppressed by acidified aspirin. Paracetamol or sodium salicylate given alone increased the generation of mucosal prostaglandin-like material. Indomethacin, the prostaglandin synthesis inhibitor, suppressed this effect and inhibited the protective influence of paracetamol or sodium salicylate on the production of gastric lesions.
D000082:Acetaminophen / Q000627:therapeutic use*; D000818:Animals; D001241:Aspirin; D011464:Epoprostenol / Q000096:biosynthesis / Q000502:physiology*; D000431:Ethanol; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012980:Sodium Salicylate / Q000627:therapeutic use*; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*
D011453:Prostaglandins; D000082:Acetaminophen; D000431:Ethanol; D011464:Epoprostenol; D001241:Aspirin; D012980:Sodium Salicylate; D007213:Indomethacin