Gastric mucosa protective effects of colloidal bismuth subcitrate (DE-NOL)

We evaluated the gastric mucosal protective properties of the anti-ulcer drug, colloidal bismuth subcitrate (CBS; DE-NOL), and its ability to stimulate mucosal synthesis of PGE2 in the rat. Gastric lesions were induced by ethanol and quantified by a visual scoring procedure. CBS was about 3-4 times more protective than sucralfate at reducing lesions. PGE2 displayed potent activity in this model, though cimetidine displayed only weak activity. Increasing the concentration of a standard dose of CBS in the rat stomach enhanced the protective activity against ethanol lesions. Pretreatment of rats with CBS led to complete, partial and no protection at 0.25, 8 and 16 h respectively. PGE2 generation in gastric mucosa biopsies was dose-dependently increased by oral CBS and peak synthesis occurred at 0.25 h. Although partial protection against ethanol lesions was found 8 h after CBS, basal levels of PGE2 generation had already returned at 4 h. Indomethacin blocked CBS-stimulated generation of PGE2, but only partially blocked the protection against ethanol-induced lesions. These findings indicated that CBS protects the rat gastric mucosa against ethanol lesions and both prostaglandin- and non-prostaglandin-mediated mechanisms could contribute to this protection.