Abstract
The pathogenesis of aspirin- or indomethacin-induced gastric and/or intestinal lesions was studied in dogs. 16,16-Dimethyl PGE2 methyl ester (16-DMPGE2) at 2 or 10 μg/kg in two divided doses given intramuscularly markedly inhibited gastric lesions produced by orally ingested aspirin at 200 mg/kg/day given twice daily for 1 or 5 days. While 16-DMPGE2 at the same dose also inhibited gastric lesions induced by a single oral administration of indomethacin at 20 mg/kg, gastric lesions including deep antral ulcers, produced by repeated administration of indomethacin, were not affected. Intestinal lesions produced by indomethacin given once, or for 5 or 10 days, were not affected. These results suggest that the lack of endogenous prostaglandins may be involved in the pathogenesis of gastric lesions produced by aspirin and indomethacin given once but may not be involved in the pathogenesis of indomethacin-induced deep lesions in the stomach and intestine.