aceglutamide-aluminum and Ulcer

Aceglutamide aluminium (AGA, KW-110, Glumal) at doses of 30-100 mg/kg p.o. prevented the formation of the gastric lesions induced by three noxious compounds, ethanol, HCl and acidified taurocholate, all dose-dependently. The preventive effect of AGA against taurocholate-induced lesions was more marked than that against the other two noxious agents. AGA at the cytoprotective doses caused almost no decrease of the gastric acid secretion in both pylorus-ligated and non-ligated rats. AGA stimulated gastric mucus secretion and prevented the increment of back-diffusion of hydrogen ion into the mucosa significantly. These data indicate that AGA caused a cytoprotective effect not through the suppression of acid secretion but through the augmentation of the defense of the mucosa against autodigestion by gastric juice. In addition, pretreatment with indomethacin diminished the cytoprotective effect of AGA almost completely. This result suggests that the mechanisms of AGA's cytoprotection may be concerned with endogenous prostaglandins.

Topics: Administration, Oral; Aluminum; Animals; Anti-Ulcer Agents; Cryoprotective Agents; Dose-Response Relationship, Drug; Ethanol; Gastric Juice; Gastric Mucosa; Glutamine; Glycoproteins; Hydrochloric Acid; Male; Organometallic Compounds; Rats; Rats, Inbred Strains; Taurocholic Acid; Time Factors; Ulcer