Bastida E, Monteagudo J, Ordinas A, De Marco L, Castillo R
Servicio Hemoterapia y Hemostasia, Facultad de Medicina, Universidad de Barcelona, Spain.
Thromb Haemost. 1988 Aug 30;60(1):30-4.
Native von Willebrand factor (N-vWF) binds to platelets activated by thrombin, ADP or ristocetin. Asialo vWF (As-vWF) induces platelet aggregation in absence of platelet activators. N-vWF mediates platelet adhesion to vessel subendothelium at high shear rates. We have investigated the role of As-vWF in supporting platelet deposition to rabbit vessel subendothelium at a shear rate of 2,000 sec-1, using the Baumgartner perfusion system. We have studied the effects of the addition of As-vWF (from 2 to 12 micrograms/ml) to perfusates consisting of washed red blood cells, 4% human albumin and washed platelets. Our results show a significant increase in platelet deposition on subendothelium (p less than 0.01) in perfusions to which As-vWF had been added. Blockage of the platelet glycoproteins Ib and IIb/IIIa (GPIb and GPIIb/IIIa) by specific monoclonal antibodies (LJIb1 and LJCP8, respectively) resulted in a decrease of platelet deposition in both types of perfusates prepared with N-vWF and As-vWF. Our results indicate that As-vWF enhances platelet deposition to vessel subendothelium under flow conditions. Furthermore, they suggest that this effect is mediated by the binding of As-vWF to platelet membrane receptors, which in turn, promote platelet spreading and adhesion to the subendothelium.
天然血管性血友病因子（N-vWF）可与由凝血酶、二磷酸腺苷（ADP）或瑞斯托菌素激活的血小板结合。去唾液酸血管性血友病因子（As-vWF）在无血小板激活剂的情况下可诱导血小板聚集。N-vWF在高剪切速率下介导血小板与血管内皮下层的黏附。我们使用鲍姆加特纳灌注系统，研究了As-vWF在剪切速率为2000秒-1时支持兔血管内皮下层血小板沉积中的作用。我们研究了向由洗涤过的红细胞、4%人白蛋白和洗涤过的血小板组成的灌注液中添加As-vWF（2至12微克/毫升）的效果。我们的结果显示，添加了As-vWF的灌注中，内皮下层的血小板沉积显著增加（p小于0.01）。用特异性单克隆抗体（分别为LJIb1和LJCP8）阻断血小板糖蛋白Ib和IIb/IIIa（GPIb和GPIIb/IIIa），导致用N-vWF和As-vWF制备的两种灌注液中的血小板沉积均减少。我们的结果表明，As-vWF在流动条件下增强了血小板向血管内皮下层的沉积。此外，结果表明这种作用是由As-vWF与血小板膜受体的结合介导的，这反过来又促进了血小板在血管内皮下层的铺展和黏附。
