Okoye B O, Losty P D, Fisher M J, Wilmott I, Lloyd D A
Department of Paediatric Surgery, Institute of Child Health, Alder Hey Children's Hospital, Liverpool.
Arch Dis Child Fetal Neonatal Ed. 1998 May;78(3):F204-8. doi: 10.1136/fn.78.3.f204.
To study the effect of prenatal glucocorticoid treatment on endothelial nitric oxide synthase (eNOS) expression in rats with congenital diaphragmatic hernia (CDH).
CDH was induced in fetal rats by the maternal administration of nitrofen on day 9.5 of gestation. Dexamethasone was administered on days 18.5 and 19.5 before delivery of the fetuses on days 20.5 and 21.5. Pulmonary eNOS protein expression was studied by western immunoblotting and immunohistochemistry.
On day 20.5, eNOS expression was significantly reduced in CDH pups compared with normal control rats. Dexamethasone treated CDH pups had eNOS concentrations equivalent to those of normal animals. By day 21.5, however, there was no detectable difference in eNOS expression between the experimental groups.
eNOS is deficient in near term (day 20.5) CDH rats. Dexamethasone restores eNOS expression in these animals to that seen in normal rat lungs. At term, the precise role of eNOS in the pathophysiology of CDH remains uncertain.
研究产前糖皮质激素治疗对先天性膈疝（CDH）大鼠内皮型一氧化氮合酶（eNOS）表达的影响。
在妊娠第9.5天给孕鼠腹腔注射硝呋烯腙诱导胎鼠发生CDH。在胎鼠于第20.5天和21.5天分娩前的第18.5天和19.5天给予地塞米松。通过蛋白质免疫印迹法和免疫组织化学研究肺组织中eNOS蛋白的表达。
在第20.5天，与正常对照大鼠相比，CDH幼鼠的eNOS表达显著降低。地塞米松治疗的CDH幼鼠的eNOS浓度与正常动物相当。然而，到第21.5天，实验组之间的eNOS表达没有可检测到的差异。
在接近足月（第20.5天）的CDH大鼠中eNOS缺乏。地塞米松可将这些动物的eNOS表达恢复到正常大鼠肺中的水平。在足月时，eNOS在CDH病理生理学中的精确作用仍不确定。
