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J Clin Gastroenterol. 1988;10 Suppl 1:S65-71.

Effects of 16,16-dimethyl-prostaglandin E2 on ammonia- and ethanol-induced mucosal lesions in the rat.

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1
Department of Geriatric Medicine, Faculty of Medicine, Kyoto University, Japan.

Abstract

The effect of necrotizing agents, such as ammonia and ethanol, on the gastric mucosa was compared. Intragastric administration of ammonia (0.6-1.0%) and ethanol (60-100%) produced hemorrhagic necrosis of gastric mucosa in a concentration-dependent manner. In the anesthetized rat, the macroscopic lesions induced by ethanol were significantly inhibited by pretreatment with 3 or 10 micrograms/kg of 16,16-dmPGE2, but the lesions induced by ammonia were not inhibited by either 3 or 10 micrograms/kg of 16,16-dmPGE2 in the anesthetized rat. The decrease of gastric transmucosal potential difference and mucosal blood flow produced by ethanol (100%) were significantly attenuated by 16,16-dmPGE2; however, those produced by ammonia (1%) were not inhibited by 16,16-dmPGE2 in the anesthetized rat. In conscious rats, ammonia-induced lesions were not inhibited by pretreatment with 3 micrograms/kg of 16,16-dmPGE2 but they were significantly reduced by the pretreatment of 10 micrograms/kg of 16,16-dmPGE2. These results show that 16,16-dmPGE2 afforded little protection against ammonia-induced gastric lesions in the anesthetized rat and suggest that a different mechanism is involved in the development of gastric mucosal lesions between those induced by ethanol and those induced by ammonia.

[Indexed for MEDLINE]

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