Hamulyák K, de Boer-van den Berg M A, Thijssen H H, Hemker H C, Vermeer C
Br J Haematol. 1987 Mar;65(3):335-8. doi: 10.1111/j.1365-2141.1987.tb06863.x.
In this paper we describe the placental transport of [3H]vitamin K1 in pregnant rats during the first 24 h after the oral administration of the vitamin. Vitamin K1 in the fetal livers ranged from 0.13% (3 h) to 2% (24 h) of the values found in the corresponding maternal livers. In spite of the low placental transfer of vitamin K, we found no accumulation of coagulation factor precursors in the fetal rat liver microsomes as could be expected in vitamin K deficiency. Moreover, we could not demonstrate any difference between adult and fetal rat liver microsomes with regard to the sensitivity for warfarin. From these results we conclude that a substantial placental barrier exists for the transport of pharmacological amounts of vitamin K1 but that under physiological conditions sufficient vitamin K1 appears to be present in the fetal liver to ensure a full carboxylation reaction. The vitamin K-dependent carboxylase activity rate of adult and fetal rat liver microsomes was comparable, indicating that the newborn rat has an adequate carboxylating system.
在本文中,我们描述了在给怀孕大鼠口服维生素后最初24小时内[3H]维生素K1的胎盘转运情况。胎肝中的维生素K1含量为相应母肝中含量的0.13%(3小时)至2%(24小时)。尽管维生素K的胎盘转运率较低,但我们并未在胎鼠肝微粒体中发现凝血因子前体的积累,而在维生素K缺乏的情况下这是可以预期的。此外,我们未能证明成年大鼠和胎鼠肝微粒体对华法林的敏感性存在任何差异。从这些结果我们得出结论,对于药理剂量的维生素K1转运存在实质性的胎盘屏障,但在生理条件下,胎肝中似乎存在足够的维生素K1以确保完全羧化反应。成年大鼠和胎鼠肝微粒体的维生素K依赖性羧化酶活性速率相当,表明新生大鼠具有足够的羧化系统。