Coller B S, Franza B R, Gralnick H R
Blood. 1976 May;47(5):841-54.
Quantitative ristocetin-induced platelet aggregation of normal platelet-rich plasma (PRP) decreased with time after PRP preparation. An increase in p H of the PRP with time proved to be responsible for this finding. Diffusion of CO2from the plasma is the prime determinant of the change in pH. Since a complex combination of factors influences CO2 diffusion (surface area-to-volume relationship, capping, mixing, etc.) The change in pH is variable with time. Thus, quantitative ristocetin aggregation should be pH controlled. A simple device for maintaining PRP pH constant by control of the ambient pCO2 was designed and found effective in keeping both pH and quantitative ristocetin aggregation constant over a prolonged period of time. It can be adapted for use in platelet aggregation studies employing other reagents. The pH dependence of ristocetin-induced platelet aggregation is consistent with other data supporting an elctrostatic interaction between the platelet, von Willebrand factor, and ristocetin. We favor a model wherein ristocetin neutralizes some of the platelet's negative change and permits the von Willebrand factor to bridge sites on separate platelets to induce agglutination.
富含血小板的正常血浆（PRP）经瑞斯托霉素诱导的定量血小板聚集在PRP制备后随时间下降。结果证明，PRP的pH值随时间升高是导致这一现象的原因。血浆中二氧化碳的扩散是pH值变化的主要决定因素。由于多种因素的复杂组合会影响二氧化碳的扩散（表面积与体积的关系、封盖、混合等），pH值随时间变化不定。因此，瑞斯托霉素定量聚集应进行pH值控制。设计了一种通过控制环境pCO₂来保持PRP pH值恒定的简单装置，发现该装置能在较长时间内有效保持pH值和瑞斯托霉素定量聚集恒定。它可适用于使用其他试剂的血小板聚集研究。瑞斯托霉素诱导的血小板聚集对pH值的依赖性与其他支持血小板、血管性血友病因子和瑞斯托霉素之间存在静电相互作用的数据一致。我们倾向于一种模型，即瑞斯托霉素中和了血小板的一些负电荷变化，并使血管性血友病因子能够连接不同血小板上的位点以诱导凝集。
