Role of gastric acid and bile acids in the pathogenesis of compound 48/80-induced gastric lesions in rats.
We studied the effects of various agents, which influence gastric acidity and bile acids, on compound 48/80 (48/80)-induced gastric lesions in rats. 48/80-Induced gastric lesions were produced by repeated intraperitoneal administration of 48/80 at 0.75 mg/kg once daily for 4 days. Test agents were given orally twice daily (30 min before and 9 hr after 48/80 administration) for 4 days. AI(OH)3 and sucralfate at 2000 mg/kg/day, a weak antacid dose, significantly inhibited (about 50-60%) the development of 48/80-induced lesions. Propantheline at 60 mg/kg/day and omeprazole at 60 or 200 mg/kg/day, which reduced gastric secretion for more than 12 hr, also significantly inhibited (about 30-40%) these lesions. Cimetidine at 200 mg/kg/day, which reduced gastric secretion for only 5 hr, had little effect on the lesion formation. Cholestyramine, which is a potent bile acids binding agent, had no effect on 48/80-induced lesions in doses of 600 or 2000 mg/kg/day. These results suggest that gastric acid, but not bile acids, is partly involved in the pathogenesis of 48/80-induced gastric lesions.
D000818:Animals; D001647:Bile Acids and Salts / Q000502:physiology*; D002792:Cholestyramine Resin / Q000494:pharmacology; D005744:Gastric Acid / Q000378:metabolism / Q000502:physiology*; D008297:Male; D051381:Rats; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000503:physiopathology; D003189:p-Methoxy-N-methylphenethylamine / Q000633:toxicity*
D001647:Bile Acids and Salts; D002792:Cholestyramine Resin; D003189:p-Methoxy-N-methylphenethylamine