Dabigatran thrombin-induced降低血小板聚集和激活方式存在剂量依赖的相关性。
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Vinholt PJ,尼尔森C, Soderstrom AC, Brandes, Nybo M
Dabigatran thrombin-induced降低血小板聚集和激活方式存在剂量依赖的相关性。
J Thromb溶栓。2017年8月,44 (2):216 - 222。doi: 10.1007 / s11239 - 017 - 1512 - 2。
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28580515 (在PubMed]
- 文摘
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Dabigatran口服抗凝剂和可逆的凝血酶抑制剂。此外,dabigatran可能影响血小板功能通过一个直接影响血小板凝血酶受体。目的是探讨dabigatran对血小板活化和血小板聚集的影响。健康供者血液孵化与dabigatran 0, 50岁,500 ng / mL,对应的治疗范围dabigatran血浆浓度峰值,和10000 ng / mL包括supra-therapeutic dabigatran等离子体水平。血小板聚集与96孔aggregometry测试。使用流式细胞仪检测血小板活化和血小板凝血酶受体表达(SPAN-12和WEDE-15表达式)。凝血酶受体激动剂,凝血酶receptor-activating肽,protease-activated receptor-4兴奋剂,胶原蛋白,collagen-related肽,花生四烯酸、腺苷二磷酸。所有浓度dabigatran完全抑制血小板聚集的凝血酶2国际单位/毫升,而由其他受体激动剂dabigatran并不影响血小板聚集。血小板激活(血小板激活GPIIb阳性的比例/ iii a, CD63, P-selectin)减少凝血酶刺激后样品与dabigatran水平> / = 500 ng / mL。与凝血酶刺激后,激活GPIIb / IIIa-positive血小板的比例是99.8 + / - 0.2%没有dabigatran, 14.7 + / - 4.7%与500 ng / mL dabigatran,和4.2 + / - 0.2% 10000 ng / mL dabigatran,两个样品没有dabigatran相比p < 0.001。 Also, the receptor expression of GPIIb/IIIa, CD63, and P-selectin were reduced after dabigatran treatment. The expression of thrombin receptors was reduced at dabigatran on >/= 500 ng/mL. In conclusion, dabigatran exclusively inhibits thrombin-induced platelet activation and aggregation with a dose-dependent response. Platelet stimulation with other agonists was not affected by dabigatran.
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