Evaluation of the effects of nicorandil on experimentally induced gastric ulcers

The present study was designed to evaluate the effects of a potassium chann el opener, nicorandil, and to elucidate its possible mechanism of action in aspirin plus pylorus ligation induced and ethanol-induced gastric ulcers i n rats. In an attempt to ascertain the involvement of K-ATP channels in the modulation of gastric ulcers, the effects of nicorandil alone as well as i n the presence of the KATP channel blocker glibenclamide were studied. Nico randil and glibenclamide were administered orally at a dose of 2 mg/kg thro ughout the study. Nicorandil showed significant protection in all the selec ted models that was evident from a significant reduction in the ulcer index . The results of nicorandil treatment were comparable with those of cimetid ine treatment in both models. Glibenclamide was found to inhibit this effec t of nicorandil. Further, glibenclamide showed proulcerogenic potential in ethanol and aspirin plus pylorus ligation models. In the aspirin plus pylor us ligation model, nicorandil showed a significant reduction in total acidi ty, pepsin activity, and protein content and a significant rise in mucin ac tivity. The effect of nicorandil was also studied on gastric mucosal blood flow (GMBF). The GMBF was found to be more increased in the test group than in the control group, indicating enhancement of GMBF by nicorandil. Gliben clamide reversed this effect of nicorandil as well. It is concluded from ou r study that nicorandil possesses antiulcer activity in the models employed in the present study. This may be attributed to the opening of KATP channe ls, inhibition of acid secretion, enhancement of mucin activity, and improv ement in GMBF. Copyright (C) 2001 S. Karger AG, Basel.