Effect of Indomethacin, Prostaglandins and Omeprazole on Healing of Experimental Gastric Ulcers

Prostaglandins and indomethacin exert trophic effects on the gastric mucosa which could be advantageous to ulcer healing. To examine the possibility of such a role, the effects of high and low doses of prostaglandin, indomethacin and omeprazole were compared in an experimental ulcer model. Gastric ulcers were induced in rats by a crypoprobe. This was followed by 5 to 10 days’ treatment with 16,16-dimethyl dinoprostone (prostaglandin E2) [5 or 100 μg/kg twice daily, intragastrically], omeprazole (40 μmol/kg once daily, subcutaneously), indomethacin (2 mg/kg twice daily, subcutaneously) or placebo. At the end of treatment, plasma gastrin levels, the size and depth of the ulcer and the labelling index in the area neighbouring the ulcer were measured. Omeprazole accelerated ulcer healing, as indicated by a smaller ulcer area and depth after 10 days’ treatment. Prostaglandins did not affect ulcer healing despite an increase in the height of the mucosa adjacent to the ulcer. Indomethacin delayed ulcer healing and reduced the labelling index of ulcer-adjacent mucosa. These observations suggest that the trophic and ‘cytoprotective’ effects of prostaglandins are not relevant for ulcer healing in this model. This is not unexpected, since the trophic effect induced by prostaglandins mainly results from an increase in the life cycle of the superficial mucus-producing cells and not by the enhancement of cell reproduction.