16-16-dimethylprostaglandin-e and Acute-Disease

Topics: Acute Disease; Administration, Topical; Antacids; Cimetidine; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Peptic Ulcer; Prostaglandins E, Synthetic; Stomach; Stress, Physiological

Acute erosions of the stomach may occur in association with human spinal cord injuries. Erosion of the glandular portion of the stomach also occurs after cervical cord transection in the rat. Reports on the effects of antacids and cimetidine in the prevention of acute "stress" erosions in animals and humans have shown conflicting results. A prostaglandin analog, 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) has been shown to prevent gastric erosions in rats produced by nonsteroid antiinflammatory compounds. Cimetidine 50 mg/kg (intraperitoneal), 16,16-dmPGE2 10 micrograms/kg (intraperitoneal), and antacid 2 ml (intragastric) were individually given to groups of spinal rats at 0 and 4 hr. 16,16-dmPGE2 and antacid both resulted in significant reduction in mean ulcer length compared to controls after 8 hr (P less than 0.05) whereas cimetidine showed no significant effect, even though cimetidine caused a significant decrease in gastric acid output compared to both 16,16-dmPGE2 and controls (P less than 0.01). It is concluded that cimetidine on this dosage schedule is not effective in the prevention of gastric erosions in a cervical cord section rat model, whereas the ulceroprotective effects of 16,16-dmPGE2 and antacids are significant. It is suggested that the gastric mucosal cells remain vulnerable to injury in the cimetidine-treated spinal rat due to secretory inhibition, but are protected by buffering action of antacids or by "cytoprotective" effects of prostaglandin.

Topics: Acute Disease; Animals; Antacids; Anti-Inflammatory Agents; Cimetidine; Gastric Acidity Determination; Gastric Mucosa; Guanidines; Injections, Intraperitoneal; Prostaglandins E, Synthetic; Rats; Rats, Inbred Strains; Spinal Cord Injuries; Stomach Ulcer