Gyires K
Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.
Arch Int Pharmacodyn Ther. 1990 Jul-Aug;306:170-81.
Morphine (0.1-2 mg/kg)--administered either orally (p.o.) or subcutaneously (s.c.)--inhibited the acidified ethanol-induced gastric damage in a dose-dependent manner. However, when morphine was given intracerebroventricularly no inhibition was observed. Naloxone (0.5 mg/kg, s.c. and p.o.) blocked the protective action of morphine. Bremazocine (0.05-1 mg/kg, p.o., s.c.) did not influence the ethanol-induced mucosal necrosis in a significant manner, but decreased (in the dose of 0.5 mg/kg, p.o., s.c.) the protective action of morphine. Morphine (1 mg/kg, s.c.) also reduced the ethanol-induced enhanced vascular permeability of gastric mucosa and naloxone (0.5 mg/kg, s.c.) inhibited this effect too. Indomethacin (10 mg/kg, p.o.) and the sulfhydryl alkylator N-ethylmaleimid (50 mg/kg, s.c.) decreased the protective action of morphine, suggesting a possible involvement of mucosal prostaglandins and sulfhydryls in the effect of morphine on ethanol-induced gastric erosions.