Jansen J W, Haverkate F, Koopman J, Nieuwenhuis H K, Kluft C, Boschman T A
Thromb Haemost. 1987 Apr 7;57(2):171-5.
We studied the influence of Factor XIIIa (F XIIIa) activity on the lysis rate of fresh whole human blood clots, without using anticoagulants. Clotting was induced by exogenous thrombin, lysis by tissue-type Plasminogen Activator (t-PA) added before clotting. After various periods of time, lysis rates were determined by measuring the radioactivity in the supernatant of the clot originating from 125I-Fibrinogen added before clotting. Lysis rates were determined in the presence of endogenous F XIIIa and compared with those obtained after specific inhibition of F XIIIa activity. We used an IgG fraction of an antiserum quenching the F XIIIa activity. Addition of increasing amounts of the antibodies to normal blood resulted in a dramatic increase in clot lysis rate, concomitant with loss of F XIII activity. Lysis of blood clots from a patient with a congenital, homozygous, functional alpha 2-Antiplasmin (alpha 2-AP) deficiency (alpha 2-AP-Enschede) was not or slightly increased by the anti F XIII antibodies indicating that fibrin-fibrin crosslinking per se does not contribute essentially to resistance of the blood clot against fibrinolysis. Both active alpha 2-AP and F XIIIa are required for the major part of the F XIII-dependent resistance of whole blood clots against lysis.
我们在不使用抗凝剂的情况下，研究了因子ⅩⅢa（FⅩⅢa）活性对新鲜人全血凝块溶解速率的影响。通过外源性凝血酶诱导凝血，在凝血前加入组织型纤溶酶原激活剂（t-PA）进行溶解。在不同时间段后，通过测量来自凝血前加入的125I-纤维蛋白原的凝块上清液中的放射性来确定溶解速率。在存在内源性FⅩⅢa的情况下测定溶解速率，并与特异性抑制FⅩⅢa活性后获得的溶解速率进行比较。我们使用了一种能淬灭FⅩⅢa活性的抗血清的IgG组分。向正常血液中添加越来越多的抗体导致凝块溶解速率显著增加，同时伴随着FⅩⅢ活性的丧失。抗FⅩⅢ抗体对一名患有先天性纯合功能性α2-抗纤溶酶（α2-AP）缺乏症（α2-AP-恩斯赫德）患者的血凝块溶解没有影响或仅有轻微增加，这表明纤维蛋白-纤维蛋白交联本身对血凝块抗纤维蛋白溶解的能力没有实质性贡献。活性α2-AP和FⅩⅢa都是全血凝块对溶解具有FⅩⅢ依赖性抵抗力的主要组成部分所必需的。
