Hubbard A R, Jennings C A
Thromb Res. 1986 May 15;42(4):489-98. doi: 10.1016/0049-3848(86)90212-4.
Factors affecting the inhibition of tissue thromboplastin (TP)-mediated blood coagulation have been investigated. Human brain thromboplastin progressively loses procoagulant activity when incubated in the presence of defibrinated plasma and CaCl2. Inhibition is maximal at a CaCl2 concentration of 1.5 mM during incubation and involves the calcium dependent binding of a plasma component(s) to the TP-FVII complex, preventing the activation of FX. Chelation of calcium ions using EDTA releases active TP and FVII from the inhibited complex. No inhibition occurs during incubation of TP with Al (OH)3 adsorbed plasma and calcium ions unless a Factor VII concentrate (or purified FVII and FX) is also present. Incubation of TP with antithrombin III-deficient plasma and calcium ions also leads to inhibition. Moreover, purified AT III cannot substitute for adsorbed plasma in producing TP inhibition. The data are consistent with the presence in plasma of a potent AT III independent inhibitor of TP-mediated blood coagulation.
对影响组织凝血活酶（TP）介导的血液凝固抑制作用的因素进行了研究。人脑海绵状血管瘤在去纤维蛋白血浆和氯化钙存在下孵育时，其促凝活性会逐渐丧失。在孵育过程中，当氯化钙浓度为1.5 mM时抑制作用最大，这涉及血浆成分与TP - FVII复合物的钙依赖性结合，从而阻止FX的激活。使用EDTA螯合钙离子可从受抑制的复合物中释放出活性TP和FVII。除非同时存在因子VII浓缩物（或纯化的FVII和FX），否则TP与吸附有Al(OH)3的血浆和钙离子孵育期间不会发生抑制作用。TP与抗凝血酶III缺乏的血浆和钙离子孵育也会导致抑制作用。此外，纯化的AT III不能替代吸附血浆来产生TP抑制作用。这些数据与血浆中存在一种有效的非AT III依赖性TP介导的血液凝固抑制剂一致。
