Silver R K, Mullen T A, Caplan M S, O'Connell P D, Ragin A
Department of Obstetrics and Gynecology, Evanston Hospital, Northwestern University Medical School, IL 60201, USA.
Am J Obstet Gynecol. 1995 Sep;173(3 Pt 1):702-7. doi: 10.1016/0002-9378(95)90326-7.
Our purpose was to determine whether anticardiolipin antibody-positive sera alter platelet adherence to vascular endothelium by a platelet activating factor-dependent mechanism.
Anticardiolipin antibody-positive sera were used in an in vitro platelet-endothelial adherence assay. Confluent endothelial monolayers were randomly assigned for exposure to a 20% concentration of experimental and control sera. Platelets were radiolabeled with chromium 51, and adherence was assessed by quantification of endothelium-associated gamma emission.
Inducible platelet adherence was observed by endothelial cell preincubation with sera from anticardiolipin antibody-positive donors compared with anticardiolipin antibody-negative control experiments (n = 12, platelet adherence 6.4% +/- 1.3% vs 4.5% +/- 1.1%, respectively; p = 0.02). Compared with endothelial cell incubations alone, coincubation of platelets with anticardiolipin antibody-positive sera consistently augmented primary adherence (n = 6, p = 0.042). Furthermore, platelet-adherence induced by antibody-positive sera was consistently attenuated by specific platelet-activating factor antagonists in a dose-dependent fashion (p < 0.001) and was restored by exogenously administered platelet-activating factor.
Anticardiolipin antibody-induced platelet adherence may constitute an important prerequisite for vascular thrombosis in antibody-positive patients. The findings from this in vitro model suggest direct involvement of platelet-activating factor in this process.
我们的目的是确定抗心磷脂抗体阳性血清是否通过血小板活化因子依赖性机制改变血小板对血管内皮的黏附。
在体外血小板 - 内皮黏附试验中使用抗心磷脂抗体阳性血清。将汇合的内皮单层随机分配用于暴露于20%浓度的实验血清和对照血清。用51铬对血小板进行放射性标记，并通过定量内皮相关的γ发射来评估黏附情况。
与抗心磷脂抗体阴性对照实验相比，抗心磷脂抗体阳性供体的血清预孵育内皮细胞后观察到可诱导的血小板黏附（n = 12，血小板黏附分别为6.4% +/- 1.3%和4.5% +/- 1.1%；p = 0.02）。与单独的内皮细胞孵育相比，血小板与抗心磷脂抗体阳性血清共同孵育持续增加初始黏附（n = 6，p = 0.042）。此外，抗体阳性血清诱导的血小板黏附被特异性血小板活化因子拮抗剂以剂量依赖性方式持续减弱（p < 0.001），并通过外源性给予血小板活化因子得以恢复。
抗心磷脂抗体诱导的血小板黏附可能是抗体阳性患者血管血栓形成的重要前提。该体外模型的研究结果表明血小板活化因子直接参与了这一过程。
