POLLER L
J Clin Pathol. 1960 May;13(3):226-9. doi: 10.1136/jcp.13.3.226.
Stored serum reduces the anticoagulant effect of heparin on the clotting times of normal plasma. This is also well marked with sera from patients with Christmas (factor IX) deficiency, with factor VII-deficient sera, and in sera derived from patients treated with phenindione with a gross defect in thromboplastin generation. The possible relationship between antiheparin activity of serum and heparin resistance in recent thrombosis is discussed. The antiheparin agent resembles factor VII and Christmas factor in being present in excess in serum, adsorbed and subsequently eluted from alumina. Unlike these, however, it does not appear to be appreciably reduced by phenindione treatment. It appears to have some properties in common with those described for the thrombotic agent of serum described by Wessler and his colleagues. It may play a part in the increased coagulability associated with thrombosis from the release of serum products into the circulation, although its relationship to the production of thrombosis in man remains to be established.
储存的血清会降低肝素对正常血浆凝血时间的抗凝作用。这在患有克里斯马斯病(因子IX缺乏)患者的血清、因子VII缺乏的血清以及接受苯茚二酮治疗且凝血活酶生成存在严重缺陷的患者血清中也表现得很明显。文中讨论了血清的抗肝素活性与近期血栓形成中肝素抵抗之间的可能关系。这种抗肝素剂与因子VII和克里斯马斯因子相似,在血清中过量存在,可被氧化铝吸附并随后洗脱。然而,与这些因子不同的是,苯茚二酮治疗似乎不会使其明显减少。它似乎具有一些与韦斯勒及其同事所描述的血清血栓形成剂相同的特性。尽管其与人血栓形成的关系尚待确定,但它可能在因血清产物释放到循环中而导致的与血栓形成相关的凝血性增加中起作用。