Mitropoulos K A, Reeves B E, O'Brien D P, Cooper J A, Martin J C
MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, Medical College of St Bartholomew's Hospital, London, UK.
Blood Coagul Fibrinolysis. 1993 Apr;4(2):223-34. doi: 10.1097/00001721-199304000-00003.
The contribution of various enzymes in the activation of factor VII, determined from the increase in factor VII coagulant activity (VIIc), was investigated following the exposure of citrated plasma to low temperature. The contact system of coagulation was initiated either by the contact surface present in certain plasmas (i.e. plasma from women in late pregnancy) or by micellar stearate added to plasma diluted with an equal volume of buffer (plasma from normal healthy subjects or from women in late pregnancy). With either of the contact surfaces, increase of VIIc and the concentration of enzymes derived from factor XII (XIIa) depended on the potency of the contact surface. The stearate-induced VIIc in diluted plasmas from women in late pregnancy or from normal subjects was inhibited by 60-70% in the presence of anti-factor IX monoclonal antibody. VIIc was not increased in XII-deficient plasma following the addition of stearate. The addition of purified human factor XII to this plasma restored the increase in VIIc and the activation of factor XII. In factor IX-deficient plasma, the stearate-induced increase in VIIc was only 38% of that seen in normal plasma and was restored by the addition of purified factor IX. Similarly in factor XI-deficient plasma, the stearate-induced increase in VIIc and the factor XII activation were 48% and 69% of that found in normal plasma. The addition of EDTA (2 mM) did not alter the extent of factor XII activation induced by contact surface, but it did inhibit the rise in VIIc. It is concluded that in the presence of contact surface the activation of factor XII and the sequential activation of factor XI and of factor IX results in the activation of factor VII. Activated factor IX is responsible for the major part of the factor VII activation whereas the rest may be through the direct activation by XIIa.
通过测定因子 VII 促凝活性（VIIc）的增加来研究不同酶在因子 VII 激活中的作用，实验在枸橼酸盐血浆暴露于低温后进行。凝血接触系统可通过某些血浆中存在的接触表面（即晚期妊娠女性的血浆）启动，也可通过向等体积缓冲液稀释的血浆中添加胶态硬脂酸盐（正常健康受试者或晚期妊娠女性的血浆）启动。无论使用哪种接触表面，VIIc 的增加以及源自因子 XII（XIIa）的酶浓度均取决于接触表面的效能。在抗因子 IX 单克隆抗体存在的情况下，晚期妊娠女性或正常受试者稀释血浆中硬脂酸盐诱导的 VIIc 被抑制 60 - 70%。添加硬脂酸盐后，XII 缺乏的血浆中 VIIc 未增加。向该血浆中添加纯化的人因子 XII 可恢复 VIIc 的增加以及因子 XII 的激活。在因子 IX 缺乏的血浆中，硬脂酸盐诱导的 VIIc 增加仅为正常血浆中的 38%，添加纯化的因子 IX 可使其恢复。同样，在因子 XI 缺乏的血浆中，硬脂酸盐诱导的 VIIc 增加以及因子 XII 激活分别为正常血浆中的 48%和 69%。添加 EDTA（2 mM）不会改变接触表面诱导的因子 XII 激活程度，但会抑制 VIIc 的升高。结论是，在存在接触表面的情况下，因子 XII 的激活以及因子 XI 和因子 IX 的顺序激活会导致因子 VII 的激活。活化的因子 IX 是因子 VII 激活的主要原因，而其余部分可能是通过 XIIa 的直接激活。
