Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland.
Thromb Res. 2011 Nov;128(5):e73-80. doi: 10.1016/j.thromres.2011.06.016. Epub 2011 Jul 23.
Platelet-leukocyte aggregation is believed to contribute to acute thrombotic events. While the effect of aspirin on platelet-to-platelet aggregation is well established, the impact of the drug on pro-inflammatory platelet function remains equivocal. Thus we investigated the effect of aspirin on selected platelet-related inflammatory biomarkers in both acute ischaemic stroke patients and healthy volunteers.
Using five-colour flow cytometry the platelet surface expression of CD62P and CD40L and subpopulations of leukocyte-platelet aggregates were assessed in 63 acute stroke patients and 40 healthy volunteers at baseline and after a 10-day period of aspirin intake at a daily dose of 150 mg. Simultaneously the plasma levels of soluble CD62P and CD40L, serum level of TxB(2), and whole blood impedance platelet aggregation under arachidonic acid (AA) stimulation were investigated.
No differences in values of studied platelet-related inflammatory biomarkers in both resting platelets and those activated with TRAP after 10-day treatment with aspirin were confirmed in stroke subjects. In healthy individuals the resting platelet expression of CD62P, plasma level of soluble CD62P and percentage of circulating monocyte-platelet aggregates were lower after the aspirin intake period (P=0.009; P=0.04; P=0.004, respectively). In both studied groups serum level of TxB(2) and platelet aggregation under AA stimulation were lower than before treatment (P<0.001).
Despite effective inhibition of COX-1-dependent platelet aggregation, aspirin does not influence the platelet α-granule-derived inflammatory mediators and monocyte-platelet aggregation in acute stroke subjects, although it does in healthy individuals.
血小板-白细胞聚集被认为有助于急性血栓事件。虽然阿司匹林对血小板-血小板聚集的作用已得到充分证实，但药物对促炎血小板功能的影响仍存在争议。因此，我们研究了阿司匹林对急性缺血性脑卒中患者和健康志愿者中选定的血小板相关炎症生物标志物的影响。
使用五色流式细胞术，在基线时和每天 150mg 剂量的阿司匹林摄入 10 天后，评估了 63 名急性脑卒中患者和 40 名健康志愿者的血小板表面 CD62P 和 CD40L 的表达以及白细胞-血小板聚集的亚群。同时，研究了可溶性 CD62P 和 CD40L 的血浆水平、血清 TxB(2)水平以及在花生四烯酸 (AA) 刺激下的全血阻抗血小板聚集。
在接受阿司匹林治疗 10 天后，在静息血小板和用 TRAP 激活的血小板中，未发现研究的血小板相关炎症生物标志物在脑卒中患者中的差异。在健康个体中，阿司匹林摄入后，静息血小板 CD62P 的表达、血浆可溶性 CD62P 的水平和循环单核细胞-血小板聚集的百分比降低（P=0.009；P=0.04；P=0.004，分别）。在两个研究组中，血清 TxB(2)水平和 AA 刺激下的血小板聚集均低于治疗前（P<0.001）。
尽管有效抑制 COX-1 依赖性血小板聚集，但阿司匹林对急性脑卒中患者的血小板α-颗粒衍生炎症介质和单核细胞-血小板聚集没有影响，尽管对健康个体有影响。
