Protection by sucralfate against indomethacin induced gastric ulceration in the guinea pig.
In the management of rheumatic diseases, peptic ulceration associated with anti-inflammatory drug therapy is a major problem and seriously limits the usefulness of these agents. In acute experiments with a guinea pig total gastric pouch preparation, gastric damage induced by the prostaglandin synthetase inhibitor indomethacin was shown to be enhanced by preliminary mucosal exposure to bile salts. In the present study, using the same preparation, we report that sucralfate, a basic aluminium salt of sucrose octasulphate, completely prevents the gastric damage observed in pouches exposed to sodium taurocholate and indomethacin. Prevention is shown not to relate solely to bile salt binding or to the weak antacid property of sucralfate.
D000535:Aluminum / Q000494:pharmacology*; D000818:Animals; D006168:Guinea Pigs; D007213:Indomethacin / Q000037:antagonists & inhibitors*; D008564:Membrane Potentials / Q000187:drug effects; D010539:Permeability; D013276:Stomach Ulcer / Q000139:chemically induced*; D013392:Sucralfate; D013656:Taurocholic Acid / Q000037:antagonists & inhibitors
D013392:Sucralfate; D013656:Taurocholic Acid; D000535:Aluminum; D007213:Indomethacin