Ethylnitrosourea(ENU)胎生期投与による先天性水頭症ラットの発生機序
スポンサーリンク
概要
- 論文の詳細を見る
The embryopathogenesis of congenital hydrocephalus remains obscure. There have been many theories proposed regarding the aqueductal patency in cases of aqueductal stenosis, in paticular on the point whether the stenotic aqueduct is the primary lesion or the consequent change due to enlarged lateral ventricles. The purpose of the present experimental study is to clarify the morphological changes of the aqueduct in fetal hydrocephalus. Pregnant Wistar rats (mean body weight at time of mating : 210g) were injected ethylnitrosourea (ENU), an intraperitoneal injection of the dosage 70mg/kg, on the gestational day 9. 5. The fetuses were sacrified daily from gestational day 10.5 to 20.5 and the brains were offered to light/electron microscopic examination. In the results, approximately 90% of the fetuses developed hydrocephalus. Degenration of matrix cells was observed as an initial morphological changes as early as on day 10.5. The degenerative changes subsided completely by day 11.5, when numerous numbers of mitotic cells appeared at the periventricular regions. It was suggested that the high proliferative tissue reactions might have a significant role to compensate the tissue damage. This reactive cell proliferation was most actively observed in the midbrain, especially in the periaqueductal area. Consequently, the aqueduct was morphologically obstracted with such parenchymatous change on day 17.5, then, enlargement of the lateral and third ventricles was identified in the later stage. There were no significant morphological changes in the choroid plexus and subarchnoid space. In conclusion, it was emphasized that the aqueductalstenosis is the primary causative lesion for development of hydrocephalus in fetuses treated with ENU administration.
- 神戸大学の論文
- 1990-06-00