Reddick R L, Griggs T R, Lamb M A, Brinkhous K M
Proc Natl Acad Sci U S A. 1982 Aug;79(16):5076-9. doi: 10.1073/pnas.79.16.5076.
The early response to coronary artery injury was investigated in normal swine and in swine with von Willebrand disease (vWD). Thirty minutes after coronary endothelial denudation, a monolayer of platelets was adherent to areas of simple injury in both bleeder and normal swine. The number of adherent platelets was not significantly different in the two phenotypes. Injury involving the media of the vessel produced platelet-fibrin thrombi. Platelet activation, as judged by pseudopod formation and platelet spreading over areas of simple injury, was significantly less in bleeder animals than in normal animals. These studies suggest that chemotaxis and initial contact adhesion of platelets to injured arterial wall is independent of the von Willebrand factor. On the other hand, the spreading and activation of platelets on the subendothelium appear to be dependent on the presence of plasma von Willebrand factor. Through this mechanism von Willebrand factor may contribute to arterial thrombosis and atherogenesis.
在正常猪和患血管性血友病（vWD）的猪中研究了对冠状动脉损伤的早期反应。冠状动脉内皮剥脱30分钟后，在出血猪和正常猪中，单层血小板均粘附于单纯损伤区域。两种表型中粘附血小板的数量无显著差异。涉及血管中膜的损伤产生血小板 - 纤维蛋白血栓。通过伪足形成和血小板在单纯损伤区域的铺展判断，出血动物中的血小板活化明显低于正常动物。这些研究表明，血小板向损伤动脉壁的趋化作用和初始接触粘附不依赖于血管性血友病因子。另一方面，血小板在内皮下的铺展和活化似乎依赖于血浆血管性血友病因子的存在。通过这种机制，血管性血友病因子可能促进动脉血栓形成和动脉粥样硬化的发生。
