Abstract
Abstract Surface hydrophobicity of the gastric mucosa and its variation in response to treatments with corticosteroids, thyroxine, and 16,16-dimethyl prostaglandin E 2 were measured in developing rats. A developmental increase in the hydrophobicity of the luminal surface of the gastric mucosa was recorded between the first and third weeks of life. The hydrophobicity of the stomach was not consistently influenced by an acute administration of 16,16-dimethyl prostaglandin E 2 (5 μg/kg, 30 min before examination) until the end of the third week of life, at which time a significant 40% increase was recorded. Similarly, the decrease in surface hydrophobicity that resulted from luminal administration of an ulcerogenic dose of HCl (0.6 N, 6 ml/kg) was blocked by 16,16-dimethyl prostaglandin E 2 only in 3-wk-old rats and not in rats 1 and 2 wk of age. Neither the normal developmental increase nor the 16,16-dimethyl prostaglandin E 2 -induced enhancement in gastric surface hydrophobicity was induced precociously by corticosterone or thyroxine. The possible importance of these findings on the development of gastric surface hydrophobicity to the ontogeny of both gastric barrier function and prostaglandin-induced gastric protection is discussed.
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