Donaldson V H, Glueck H I, Miller M A, Movat H Z, Habal F
J Lab Clin Med. 1976 Feb;87(2):327-37.
Plasma from an asymptomatic person with defects in blood coagulation, release of kinin, and evolution of fibrinolytic activity upon contact with a foreign surface was deficient in kininogen. The coagulation defect was identified as "Fitzgerald trait." A preparation of high molecular weight kininogen repaired the defects in clotting, kinin release and fibrinolysis, but a preparation of low molecular weight kininogen did not. Therefore, Fitzgerald factor appears to be a high molecular weight kininogen. The site of action of the kininogen appears to be after that of activated Hageman factor and kallikrein in the generation of clot-promoting activity through activation of plasma thromboplastin antecedent (PTA).
一名无症状但存在血液凝固缺陷、激肽释放以及接触异物表面时纤溶活性变化的人的血浆中激肽原缺乏。这种凝血缺陷被确定为“菲茨杰拉德特征”。高分子量激肽原制剂修复了凝血、激肽释放和纤溶方面的缺陷，但低分子量激肽原制剂则不能。因此，菲茨杰拉德因子似乎是一种高分子量激肽原。在通过激活血浆凝血活酶前体（PTA）产生促进凝血活性的过程中，激肽原的作用位点似乎在活化的哈格曼因子和激肽释放酶之后。
