Scott J P, Montgomery R R
Blood. 1981 Dec;58(6):1075-80.
von Willebrand's antigen II (vW AgII), a plasma and platelet antigen immunologically and biochemically distinct from factor-VIII-related antigen (VIIIR:Ag), is decreased in von Willebrand's disease. vW AgII is released from platelets during aggregation and clotting. The release of platelet vW AgII was studied in washed platelets following aggregation by thrombin, collagen, and adenosine diphosphate (ADP). Total platelet vW AgII was 3.39 U/10(9) platelets. Thrombin and collagen yielded release of 85% and 86% of platelet vW AgII, respectively, at the highest concentrations. Release of platelet vW AgII was correlated with the release of 5-hydroxytryptamine (5HT). Release of vW AgII by collagen and thrombin was inhibited by metabolic inhibitors. In addition, collagen release of vW AgII was inhibited by aspirin. In clinical syndromes associated with intravascular platelet destruction, marked elevations of plasma vW AgII were noted. Thus, vW AgII is released by a metabolically active process from platelets during aggregation. In addition, vW AgII appears to be a marker of intravascular platelet destruction.
血管性血友病因子抗原II(vW AgII)是一种在免疫学和生物化学性质上与VIII因子相关抗原(VIIIR:Ag)不同的血浆和血小板抗原,在血管性血友病中含量降低。vW AgII在血小板聚集和凝血过程中从血小板释放出来。在经凝血酶、胶原和二磷酸腺苷(ADP)诱导聚集后的洗涤血小板中研究了血小板vW AgII的释放情况。血小板vW AgII的总量为3.39 U/10⁹个血小板。在最高浓度时,凝血酶和胶原分别使85%和86%的血小板vW AgII释放出来。血小板vW AgII的释放与5-羟色胺(5HT)的释放相关。胶原和凝血酶诱导的vW AgII释放受到代谢抑制剂的抑制。此外,阿司匹林可抑制胶原诱导的vW AgII释放。在与血管内血小板破坏相关的临床综合征中,观察到血浆vW AgII显著升高。因此,vW AgII在聚集过程中通过代谢活跃的过程从血小板释放出来。此外,vW AgII似乎是血管内血小板破坏的一个标志物。