Treatment of established spinal injury-induced gastric erosions in rats with cimetidine and 16,16-dimethyl prostaglandin E2.

Most research on the beneficial effects of pharmacologic agents on stress-induced acute gastric erosions in animals is directed at prevention. It is only the rare study that has been concerned with treatment of established erosions. A treatment model has been created using cervical cord-injured male Sprague-Dawley rats which consistently developed extensive linear erosions of the glandular portions of the stomach within 12 hr. A group of spinal rats was sacrificed after 12 hr to serve as a base of pretreatment ulcer severity. Treatment of established erosions with cimetidine 25 mg/kg every 2 hr in one group and 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) 5 micrograms/kg every 2 hr in a second group was compared to saline-treated controls. All drugs were administered by intraperitoneal route. Treatment began 12 hr after the cord transection and continued for another 12 hr at which time the rats were sacrificed. Both cimetidine and 16,16-dmPGE2 significantly inhibited the degree of erosion progression after 12 hr compared to saline controls (P less than 0.05). Acid output studies were carried out on a second set of rats subjected to the same experimental conditions with the addition of pyloric ligation 6 hr prior to sacrifice. A significant decrease in acid output (P less than 0.05) occurred only in the cimetidine group compared to control. It is concluded that both cimetidine and 16,16-dmPGE2 can arrest the progression of erosive changes in the stomach after cervical cord injury in rats. This is likely related to acid reduction by cimetidine and cytoprotection by prostaglandin.