Burman J F, Chung H I, Lane D A, Philippou H, Adami A, Lincoln J C
Department of Haematology, Royal Brompton Hospital, London, UK.
Lancet. 1994 Oct 29;344(8931):1192-3. doi: 10.1016/s0140-6736(94)90509-6.
During cardiopulmonary bypass, thrombin is generated, which is thought to be initiated by activation of factor XII on the surface of the bypass equipment. We present a patient with severe factor XII deficiency who underwent cardiac surgery. As much thrombin was formed during cardiopulmonary bypass (measured by the prothrombin activation fragment F1 + 2 and thrombin-antithrombin complexes) as in normal patients, showing that factor XII was not necessary for thrombin generation. Factor X, but not factor IX, was activated (as measured by their activation peptides), and this activation correlated with F1 + 2 and thrombin-antithrombin complexes, suggesting that the tissue-factor/factor-VIIa pathway is the trigger for thrombin formation.
在体外循环期间，会产生凝血酶，据认为这是由体外循环设备表面的因子 XII 激活引发的。我们报告了一名患有严重因子 XII 缺乏症的患者接受了心脏手术。在体外循环期间形成的凝血酶量（通过凝血酶原激活片段 F1 + 2 和凝血酶 - 抗凝血酶复合物测量）与正常患者一样多，这表明因子 XII 对于凝血酶生成并非必需。因子 X 而非因子 IX 被激活（通过其激活肽测量），并且这种激活与 F1 + 2 和凝血酶 - 抗凝血酶复合物相关，表明组织因子/因子 VIIa 途径是凝血酶形成的触发因素。
