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用狼疮凝集抑制物（ＬＣＩ）阳性的病人血清、亲和分离的ＩｇＧ和脂质体亲和纯化的抗心磷脂抗体（ＡＣＡ）作用于人内皮细胞（ＥＣ），测定ＥＣ释放的前列环素（ＰＧＩ＿２）。结果表明，对照组ＰＧＩ＿２的平均释放量为１３０５±２４０ｐｇ／ｍｌ，实验组为１２４６±２８７ｐｇ／ｍｌ，差别为４．５％（Ｐ＞０．０５）。经人α－凝血酶（１Ｕ／ｍｌ）刺激后，对照组ＥＣ释放ＰＧＩ＿２的量平均增加２．１倍，实验组为１．３６倍，差别为３５．２％（Ｐ（０．０５）。上述三种成份均能明显抑制低浓度凝血酶（１Ｕ／ｍｌ）介导ＥＣ释放ＰＧＩ＿２，但并不抑制高浓度凝血酶（１０Ｕ／ｍｌ）和花生四烯酸（２０μｍｏｌ／ｍｌ）介导ＥＣ释放ＰＧＩ＿２（Ｐ＞０．０５）。因此，具有ＬＣＩ活性的ＡＣＡ对凝血酶介导的ＥＣ释放ＰＧＩ＿２的抑制是引发血栓形成的机制之一；也是现所知的直接沟通免疫和凝血两大系统的唯一抗体。
Human endothelial cells (ECs) were treated with sera from patients positive for lupus-coagulation inhibitor (LCI), affinity-separated IgG, and liposome-affinity purified anti-cardiolipin antibodies (ACA) PGI_2). The results showed that the average release of PGI_2 in the control group was 1305 ± 240 pg / ml, and the experimental group was 1246 ± 287 pg / ml, with a difference of 4.5% (P> 0.05). After stimulated by human α-thrombin (1U / ml), the amount of PGI2 released by the control group increased by an average of 2.1-fold and 1.36-fold, respectively, with a difference of 35.2% (P <0.05). All of the above three components could significantly inhibit the release of PGI2 by low concentration of thrombin (1U / ml), but did not inhibit the release of EC by high concentration of thrombin (10U / ml) and arachidonic acid (20μmol / ml) PGI_2 (P> 0.05). Therefore, inhibition of PGI_2 by thrombin-mediated EC release by ACA with LCI activity is one of the mechanisms that lead to thrombosis. It is also known that the direct communication of immune and coagulation of two major systems The only antibody.