OPTIMIZATION OF CONDITIONS FOR THE CATALYTIC EFFECT OF THE FACTOR-IXA - FACTOR-VIII COMPLEX - PROBABLE ROLE OF THE COMPLEX IN THE AMPLIFICATION OF BLOOD-COAGULATION

OPTIMIZATION OF CONDITIONS FOR THE CATALYTIC EFFECT OF THE FACTOR-IXA - FACTOR-VIII COMPLEX - PROBABLE ROLE OF THE COMPLEX IN THE AMPLIFICATION OF BLOOD-COAGULATION
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DOI:
10.1016/0049-3848(79)90172-5
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发表时间:
1979-01-01
影响因子:
7.5
通讯作者:
VARADI, K
VARADI, K
中科院分区:
医学3区
文献类型:
--
作者:
ELODI, S;VARADI, K

文献摘要

被引文献

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纯化的人因子IXa激活因子X在血浆中仅为中等程度。如果因子IXa与因子VIII、磷脂和Ca形成复合物,则因子IXa的活性增加约20倍。微量的因子VIII可增强因子IXa的活性。激活因子X的量与复合物的IXa浓度直接相关。低于0.3 U[单位]/ml的因子IXa浓度,相对过量的Ca,例如30 mM CaCl2抑制了复合物的功能。通过降低Ca的浓度,即使在低因子IXa浓度下,也可以获得大约20倍的最大活性增加。在1 U/ml的IXa因子、1 U/ml的VIII因子、40 .mu的组合下,复合物的活性最大。g/ml磷脂和30mm CaCl2。在这种情况下,1 mol的因子IXa在30秒内激活23 mol的因子X。在最大活性复合物的情况下,从因子XI的激活到纤维蛋白的形成,计算出大约108的放大值。根据实验结果和内在凝血因子激活动力学,讨论了IXa和VIII因子复合物在凝血生理病理过程中的作用。
Purified human factor IXa activated factor X in the plasma only to a moderate extent. The activity of factor IXa was increased about 20-fold, if factor IXa formed a complex with factor VIII, phospholipid and Ca. Minute amounts of factor VIII enhanced the activity of factor IXa. The amount of activated factor X was directly related to the IXa concentration of the complex. Below 0.3 U[units]/ml factor IXa concentration the relative excess of Ca, e.g., 30 mM CaCl2 inhibited the functioning of the complex. By decreasing the concentration of Ca an approximate 20-fold maximal activity increment can be attained even at low factor IXa concentation. The complex displayed maximal activity at the following composition: 1 U/ml factor IXa, 1 U/ml factor VIII, 40 .mu.g/ml phospholipid and 30 mM CaCl2. Under such circumstances 1 mol of factor IXa activated 23 mol of factor X in 30 s. In the case of a maximally active complex an approximately 108 amplification value was calculated from the activation of factor XI to the formation of fibrin. In light of the experimental results and of the kinetics of activation of intrinsic clotting factors, the role of the complex of factors IXa and VIII in the physiological and pathological processes of blood coagulation was discussed.