Bauer K A, Eichinger S, Mannucci P M, Rosenberg R D
Hematology-Oncology Section, Department of Medicine, Brockton-West Roxbury Department of Veterans Affairs Medical Center, Massachusetts 02132, USA.
Haemostasis. 1996;26 Suppl 1:72-5. doi: 10.1159/000217244.
To evaluate the mechanism responsible for the generation of factor VIIa in vivo, we measured the levels of this enzyme after administering purified factor IX concentrates to patients with hemophilia B. Their factor VIIa levels were initially very low and gradually increased to normal, but there were no significant changes in the generation of factor Xa or thrombin. The administration of 10 mu g/kg body weight of recombinant factor VIIa to patients with factor VII deficiency increased the circulating levels 35-fold, but this only resulted in normalization of the activation of factor IX and factor X. Our data indicate that factor IXa is primarily responsible for the basal levels of free factor VIIa in vivo, and that changes in free factor VIIa in the blood do not necessarily lead to alterations in factor X activation.
为评估体内因子VIIa生成的机制，我们在给B型血友病患者输注纯化的因子IX浓缩物后测量了该酶的水平。他们的因子VIIa水平最初非常低，随后逐渐升至正常水平，但因子Xa或凝血酶的生成没有显著变化。给因子VII缺乏症患者静脉注射10μg/kg体重的重组因子VIIa后，循环水平升高了35倍，但这仅使因子IX和因子X的激活恢复正常。我们的数据表明，因子IXa是体内游离因子VIIa基础水平的主要原因，血液中游离因子VIIa的变化不一定会导致因子X激活的改变。
