Lalau Keraly C, Delautier D, Delabassee D, Chignard M, Benveniste J
Thromb Res. 1984 Jun 15;34(6):463-71. doi: 10.1016/0049-3848(84)90251-2.
Ticlopidine was incubated in vitro with rabbit or human washed platelets and aggregations were triggered by submaximal concentrations of adenosine-5'-diphosphate (ADP), arachidonic acid (AA) and Paf-acether (platelet-activating factor), the mediators of the three known pathways of platelet activation. Inhibition of Paf-acether-induced rabbit platelet aggregation was proportional to the concentrations of Ticlopidine used. The same range of inhibition by Ticlopidine was observed when aggregations were triggered by the two other agonists. Human platelet aggregation induced by Paf-acether was also inhibited by Ticlopidine. Inhibition was increased when platelets were rendered insensitive to ADP and AA. Our results show that Ticlopidine inhibits human and rabbit platelet aggregation triggered by Paf-acether through a mechanism not related to the inhibition of the ADP and prostaglandin pathways.
噻氯匹定与兔或人的洗涤血小板在体外进行孵育,血小板聚集由亚最大浓度的5'-二磷酸腺苷(ADP)、花生四烯酸(AA)和血小板活化因子(Paf-乙酰醚)触发,这三种物质是已知的三种血小板活化途径的介质。噻氯匹定对Paf-乙酰醚诱导的兔血小板聚集的抑制作用与所用噻氯匹定的浓度成正比。当由其他两种激动剂触发聚集时,也观察到了噻氯匹定相同范围的抑制作用。Paf-乙酰醚诱导的人血小板聚集也受到噻氯匹定的抑制。当血小板对ADP和AA不敏感时,抑制作用增强。我们的结果表明,噻氯匹定通过一种与抑制ADP和前列腺素途径无关的机制抑制Paf-乙酰醚触发的人和兔血小板聚集。