Evaluation of anti-platelet aggregatory effects of aspirin, cilostazol and ramatroban on platelet-rich plasma and whole blood
Evaluation of anti-platelet aggregatory effects of aspirin, cilostazol and ramatroban on platelet-rich plasma and whole blood
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DOI：
10.1097/00001721-200403000-00007
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发表时间：
2004-03-01
影响因子：
1.1
通讯作者：
Yamada, K
中科院分区：
文献类型：
--
作者：
Kariyazono, H;Nakamura, K;Yamada, K
为了比较阿司匹林（一种环氧化酶抑制剂）、西洛他唑（一种磷酸二酯酶III抑制剂）和雷马托班（一种特异性血栓素a(2)受体拮抗剂）的抗血小板作用，我们测量了二磷酸腺苷（ADP）、胶原和花生四烯酸诱导的人富血小板血浆（PRP）聚集以及ADP诱导的全血（WB）聚集。我们还研究了p -选择素、转化生长因子- β 1的释放和血栓素A(2)的形成对激动剂的反应。100 μ mol/l阿司匹林、10 μ mol/l西洛他唑和1 μ mol/l雷曲班对5 μ mol/l adp诱导的PRP聚集的抑制作用相似。然而，与其他药物相比，阿司匹林对5 μ mol/l ADP的反应强烈抑制血栓素A(2)的形成。10 μ mol/l西洛他唑对PRP聚集和分子释放的抑制作用在三种激动剂诱导的反应性上非常相似。阿司匹林和西洛他唑以浓度依赖的非线性方式抑制血小板聚集，而拉马托班则随着浓度的增加呈线性抑制。通过测量三种激动剂诱导的PRP聚集，以及测量WB聚集，可以清楚地证明具有不同药理机制的药物的抗血小板作用，WB聚集很可能不仅反映血小板-血小板相互作用，还反映血小板-白细胞相互作用，以及血小板内分子的释放。(C) 2004利平科特·威廉姆斯·威尔金斯。
To compare property in anti-platelet effects of aspirin (a cyclooxygenase inhibitor), cilostazol (a phosphodiesterase III inhibitor) and ramatroban (a specific thromboxane A(2) receptor antagonist), we measured human platelet-rich plasma (PRP) aggregation induced by adenosine diphosphate (ADP), collagen and arachidonic acid, and whole blood (WB) aggregation induced by ADP. The release of P-selectin, transforming growth factor-beta 1, and the formation of thromboxane A(2) in response to agonists were also investigated. Inhibitory effects of 100 mumol/l aspirin, 10 mumol/l cilostazol and 1 mumol/l ramatroban on 5 mumol/l ADP-induced PRP aggregation were similar. However, aspirin strongly inhibited thromboxane A(2) formation in response to 5 mumol/l ADP compared with other drugs. Inhibitory effects of 10 mumol/l cilostazol on PRP aggregation and the release of molecules were quite similar in responsiveness induced by the three agonists. Aspirin and cilostazol inhibited platelet aggregation in a concentration-dependent, non-linear fashion, while ramatroban inhibited linearly with increasing concentration. Anti-platelet effects of drugs having different pharmacological mechanisms were demonstrated clearly by measuring PRP aggregation induced by the three agonists, and by measuring WB aggregation that most probably reflects not only platelet-platelet interactions, but also platelet-leukocyte interactions, as well as the release of intraplatelet molecules. (C) 2004 Lippincott Williams Wilkins.