Hathaway W E, Christian J, McGregor R, Borden C
Thromb Res. 1982 Feb 1;25(3):267-75. doi: 10.1016/0049-3848(82)90246-8.
Using a rabbit anti-human prekallikrein antibody crossed immunoelectrophoresis (CIE) and Laurell rocket antigen determinations were done in plasma of subjects with Fletcher (prekallikrein, PKA), Fitzgerald (high molecular weight kininogen), Hageman (XII), and PTA (XI) deficiencies as well as in patients with activation of coagulation (intravascular coagulation syndromes). Abnormal CIE patterns were seen in the Fletcher and Fitzgerald deficient plasmas and also in some of the patients with intravascular coagulation. In vitro studies of plasma treated with thrombin, plasmin, and contact activating agents indicated that abnormal CIE patterns and increased PKA antigen levels were indicative of activation of the Hageman factor dependent pathway and not the result of plasma clotting by thrombin. In vivo activation of the Hageman factor dependent pathway frequently results in an abnormal CIE and a low PKA antigen level.
使用兔抗人前激肽释放酶抗体进行交叉免疫电泳(CIE),并对患有弗莱彻(前激肽释放酶,PKA)、菲茨杰拉德(高分子量激肽原)、哈格曼(XII)和PTA(XI)缺乏症的受试者血浆以及凝血激活患者(血管内凝血综合征)进行Laurell火箭抗原测定。在弗莱彻和菲茨杰拉德缺乏症血浆以及一些血管内凝血患者中观察到异常的CIE模式。对用凝血酶、纤溶酶和接触激活剂处理的血浆进行的体外研究表明,异常的CIE模式和PKA抗原水平升高表明哈格曼因子依赖性途径被激活,而不是凝血酶导致血浆凝固的结果。体内哈格曼因子依赖性途径的激活经常导致异常的CIE和低PKA抗原水平。