Dial E J, Lichtenberger L M
Department of Physiology and Cell Biology, University of Texas Medical School at Houston.
Gastroenterology. 1988 Jan;94(1):57-61. doi: 10.1016/0016-5085(88)90609-9.
Surface hydrophobicity of the gastric mucosa and its variation in response to treatments with corticosteroids, thyroxine, and 16,16-dimethyl prostaglandin E2 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 E2 (5 micrograms/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 E2 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 E2-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.
在发育中的大鼠中,测量了胃黏膜的表面疏水性及其对皮质类固醇、甲状腺素和16,16 - 二甲基前列腺素E2治疗的反应变化。在出生后的第一周和第三周之间,记录到胃黏膜腔表面的疏水性有发育性增加。直到出生后第三周结束,急性给予16,16 - 二甲基前列腺素E2(5微克/千克,检查前30分钟)对胃的疏水性没有持续影响,此时记录到疏水性显著增加了40%。同样,致溃疡剂量的HCl(0.6 N,6毫升/千克)经腔内给药导致的表面疏水性降低,仅在3周龄大鼠中被16,16 - 二甲基前列腺素E2阻断,而在1周龄和2周龄大鼠中未被阻断。皮质酮或甲状腺素均未过早诱导胃表面疏水性的正常发育性增加或16,16 - 二甲基前列腺素E2诱导的增强。讨论了这些关于胃表面疏水性发育的发现对胃屏障功能个体发育和前列腺素诱导的胃保护的可能重要性。