Cattaneo M, Bevilacqua C, Lecchi A, Mannucci P M
A Bianchi Bonomi Hemophilia and Thrombosis Center, Italy.
Haemostasis. 1987;17(5):293-300. doi: 10.1159/000215758.
We have done a comprehensive study in normal volunteers of the in vitro and ex vivo effects of the antiplatelet agent indobufen on platelet aggregation, the release reaction and thromboxane B2 (TxB2) production as induced by different concentrations of aggregating agents. At low concentrations (10 microM), indobufen completely inhibited secondary platelet aggregation, the release reaction and TxB2 production stimulated by ADP, epinephrine and low concentrations of platelet-activating factor (PAF acether). Higher concentrations of indobufen (100 microM) completely inhibited TxB2 production, platelet aggregation and ATP release induced by arachidonic acid (1 mM) or collagen (2 micrograms/ml). The inhibitory effect was partially overcome by higher concentrations of arachidonic acid (2 mM). Data obtained ex vivo 2 h after the oral administration of 200 mg indobufen to 8 normal volunteers were in keeping with those of the in vitro study. We conclude that indobufen inhibits platelet aggregation and the release reaction by inhibiting the platelet arachidonate pathway.
我们对正常志愿者进行了一项全面研究，观察抗血小板药物吲哚布芬对不同浓度聚集剂诱导的血小板聚集、释放反应和血栓素B2（TxB2）生成的体外和离体效应。在低浓度（10微摩尔）时，吲哚布芬完全抑制了由ADP、肾上腺素和低浓度血小板活化因子（PAF乙酰醚）刺激引起的继发性血小板聚集、释放反应和TxB2生成。较高浓度的吲哚布芬（100微摩尔）完全抑制了由花生四烯酸（1毫摩尔）或胶原（2微克/毫升）诱导的TxB2生成、血小板聚集和ATP释放。较高浓度的花生四烯酸（2毫摩尔）可部分克服这种抑制作用。对8名正常志愿者口服200毫克吲哚布芬2小时后获得的离体数据与体外研究结果一致。我们得出结论，吲哚布芬通过抑制血小板花生四烯酸途径来抑制血小板聚集和释放反应。
