Owen C A, Bowie E J
Haemostasis. 1978;7(4):189-201. doi: 10.1159/000214261.
When rats were given single or multiple doses of warfarin, the levels of prothrombin and factors VII, IX, and X were depressed, as expected. However, modest reductions of factors V, VIII, XI, and XII, but not of fibrinogen, also occurred. The levels of all eight factors promptly returned to normal when vitamin K1 was given. Warfarin-resistant rats had no depression of any of the eight factors. When vitamin K deficiency was induced by internal or external biliary fistula, factors II-VII-IX-X decreased sharply and factors V-VIII-XI-XII decreased modestly. Again, all depression were promptly reversed by vitamin K1. Isolated livers from warfarinized rats did not generate the classic vitamin K-dependent factors during 5 h of perfusion but did generate small amounts of factors V, XI, and XII, although less than normal. The isolated rat liver apparently does not generate factor VIII.
给大鼠单次或多次给予华法林后,凝血酶原以及Ⅶ、Ⅸ和Ⅹ因子的水平如预期那样降低。然而,Ⅴ、Ⅷ、Ⅺ和Ⅻ因子也出现了适度降低,但纤维蛋白原未降低。给予维生素K1后,所有这八种因子的水平迅速恢复正常。对华法林耐药的大鼠,这八种因子均未降低。当通过内或外胆瘘诱发维生素K缺乏时,Ⅱ-Ⅶ-Ⅸ-Ⅹ因子急剧下降,Ⅴ-Ⅷ-Ⅺ-Ⅻ因子适度下降。同样,维生素K1能迅速逆转所有这些因子的降低。来自用华法林处理过的大鼠的离体肝脏在灌注5小时期间不会生成典型的维生素K依赖因子,但会生成少量的Ⅴ、Ⅺ和Ⅻ因子,尽管比正常情况少。离体大鼠肝脏显然不会生成Ⅷ因子。