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抗血小板药物研究进展 被引量：2

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摘要 冠心病已成为危害人类健康的首要疾病，冠心病的发病机制比较复杂，研究表明，其发生发展与血小板过度活化关系密切。在正常的血液循环中，血小板为静息状态，而当血管内皮损伤或是动脉粥样硬化斑块破裂，内皮下的基质暴露，出现活化因子时，血小板将由静息状态转为功能状态，即血小板的激活；然后血小板粘附介导的血管性血友病因子（ vWF）与血小板膜糖蛋白（ GP） IB结合，形成vWF-GP IB，在损伤处形成一层血小板膜，二级介质如二磷酸腺苷（ ADP）与血小板膜上ADP受体相结合，从而改变血小板表面构型，形成GP11 b／IIIa受体，血小板之间即可通过该受体与纤维蛋白原相互连接，即血小板的粘附与聚集［1］。其中导致血小板表面构型改变的物质称为诱导剂，除ADP外，常见的还有血栓素A2（ TXA2）、凝血酶、胶原、免疫复合物和某些药物等。抗血小板药物可作用于其中任一环节，以下将按不同的抗血小板机制介绍几种目前临床常用的抗血小板药物。
作者 洪芳德 王邦宁
机构地区 安徽医科大学第一附属医院心血管内科
出处 《中国临床保健杂志》 CAS 2014年第1期110-112,共3页 Chinese Journal of Clinical Healthcare
关键词 抗血小板药物 血小板膜糖蛋白 动脉粥样硬化斑块破裂 血管内皮损伤 ADP受体 血管性血友病因子 血小板粘附 血小板表面
分类号 R97 [医药卫生—药品]
  • 相关文献

参考文献16

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二级参考文献39

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共引文献93

同被引文献37

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引证文献2

二级引证文献4

中国临床保健杂志
2014年 第1期

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