Peters P W, Verhoef A, Hagenaars A M
Acta Morphol Neerl Scand. 1981 Sep;19(3):205-16.
During the complete fetal period alpha-fetoprotein (AFP) was quantified in maternal sera and amniotic fluid from control, hypervitaminosis A and trypan blue treated normal rat fetuses, and from exencephalic and spina bifida aperta fetuses. The occurrence of histologic proven open neural tube defects was associated with amniotic fluid AFP levels that were much elevated over those of control and treated normal fetuses and those with closed neural tube defects at nearly the whole fetal period. In combining these results with the earlier reported morphologic data of the same rat fetuses as used in the present study, it is concluded that the elevation of amniotic AFP is caused by leakage of fetal serum through a disrupted and necrotic nervous tissue into the amniotic fluid. This experimental model of induced neural tube defects results in increase of amniotic fluid AFP levels similar to those found in human amniotic fluid in the presence of neural tube defects.
在整个胎儿期,对对照组、维生素A过多症组、锥虫蓝处理的正常大鼠胎儿以及无脑儿和脊柱裂开放性胎儿的母血清和羊水中的甲胎蛋白(AFP)进行了定量分析。经组织学证实的开放性神经管缺陷的发生与羊水AFP水平有关,在几乎整个胎儿期,该水平比对照组、处理过的正常胎儿以及患有闭合性神经管缺陷的胎儿的羊水AFP水平高得多。将这些结果与本研究中使用的相同大鼠胎儿的早期报告的形态学数据相结合,可以得出结论,羊水AFP升高是由于胎儿血清通过受损和坏死的神经组织渗漏到羊水中所致。这种诱导神经管缺陷的实验模型导致羊水AFP水平升高,类似于在存在神经管缺陷的人类羊水中发现的水平。