Nunn B
Thromb Res. 1983 Sep 1;31(5):657-63. doi: 10.1016/0049-3848(83)90096-8.
A technique is described that renders human platelets totally insensitive to synthetic PAF. The procedure involves gently mixing human citrated platelet-rich plasma (PRP) with 0.1 microM PAF at room temperature. After 3-5 min, a further addition of 0.1 microM PAF is made, followed 3-5 min later by 1 microM PAF. Preparations so treated did not aggregate in response to 50 microM PAF whereas control PRP always responded to 0.05 microM PAF. The selectivity of the desensitisation procedure depended on the presence of aspirin. In the absence of aspirin, collagen-induced aggregation was slightly inhibited, but so too was primary aggregation in response to ADP and the thromboxane receptor agonist, U46619. When PRP was pretreated with aspirin to prevent any secondary aggregation during the desensitisation procedure, collagen-induced aggregation and primary aggregation in response to ADP were essentially unchanged by total desensitisation to PAF. It is concluded that endogenous PAF acting extracellularly does not mediate or help to mediate collagen-induced aggregation in human citrated PRP.
本文描述了一种使人类血小板对合成血小板活化因子(PAF)完全不敏感的技术。该程序包括在室温下将人类枸橼酸化富血小板血浆(PRP)与0.1微摩尔/升的PAF轻轻混合。3 - 5分钟后,再加入0.1微摩尔/升的PAF,3 - 5分钟后接着加入1微摩尔/升的PAF。经过如此处理的制剂对50微摩尔/升的PAF无聚集反应,而对照PRP对0.05微摩尔/升的PAF总是有反应。脱敏程序的选择性取决于阿司匹林的存在。在没有阿司匹林的情况下,胶原诱导的聚集略有抑制,但对ADP和血栓素受体激动剂U46619的初级聚集也受到抑制。当PRP用阿司匹林预处理以防止脱敏程序期间的任何二次聚集时,对PAF完全脱敏后,胶原诱导的聚集和对ADP的初级聚集基本未变。得出的结论是,细胞外起作用的内源性PAF不介导或有助于介导人类枸橼酸化PRP中胶原诱导的聚集。