PLATELET ANTIGENS AND PLATELET ACTIVATION

我们已经开发了几种方法来研究离体血小板活化， 在体外。这些研究之所以成为可能， 实施从人血中分离血小板的技术， 诱导血小板活化或分泌。我们已经开发了九（9） 单克隆抗体仅与活化的血小板反应。我们 结果显示在某些形式的血管性血友病中， 存在血小板活化并引起血小板减少症。患者 动脉粥样硬化性心脏病患者，运动后血小板活化， 增加这表明，一定程度的血小板活化发生在 这些患者在剧烈运动后。志愿者接受 内毒素、自发血小板活化或增强激动剂诱导的 未观察到血小板活化。运动在个人与轻微或 轻度动脉粥样硬化不诱导血小板活化。 我们已经确定了阵发性睡眠性血红蛋白尿症（pNH）患者 血小板活化激活是通过释放α 颗粒蛋白和增加的纤维蛋白原与血小板的结合 面观察到凝血激活的新证据。这些 研究结果表明，血小板活化可能是主要的机制， PNH中的静脉血栓形成。测试这一假设的研究在 正在实施的过程。我们还发现了α- 体外活化血小板上的颗粒蛋白。

We have developed several methods to study platelet activation ex-vivo and in-vitro. These studies were made possible by the development and implementation of techniques to isolate platelets from human blood without inducing platelet activation or secretion. We have developed nine (9) monoclonal antibodies which react only with activated platelets. Our results have shown that in some forms of von Willebrand's disease, platelet activation is present and causes thrombocytopenia. In patients with arteriosclerotic heart disease, after exercise platelet activation is increased. This suggests that some degree of platelet activation occurs in these patients following strenuous exercise. In volunteers receiving endotoxin, spontaneous platelet activation or enhanced agonist-induced platelet activation is not observed. Exercise in individuals with minor or mild atherosclerosis does not induce platelet activation. We have identified patients with paroxysmal nocturnal hemoglobinuria (pNH) platelet activation. The activation was determined by release of alpha granule protein and the increased fibrinogen binding to the platelet surface. New evidence of coagulation activation was observed. These finding suggest that platelet activation may be the primary mechanism of venous thrombosis in PNH. Studies to test this hypothesis are in the process of being implemented. We have also identified modulation of alpha- granule proteins on platelets activated in-vitro.