發(fā)布時(shí)間：2019-07-28 14:14

【摘要】：正當(dāng)血管壁受損時(shí),人體會(huì)啟動(dòng)止血途徑來(lái)保護(hù)損傷的血管,但是抗凝血因子超出了正常調(diào)控范圍,參與凝血的物質(zhì)就會(huì)積聚于血管壁,導(dǎo)致病理性血栓形成�？寡“逅幨侵委熝ǖ囊活愔匾乃幬�,其主要以血小板聚集過(guò)程中的某些關(guān)鍵物質(zhì)或信號(hào)途徑作為治療靶標(biāo),下調(diào)血小板整合素αⅡbβ3(GPⅡbⅢa)的黏附功能,達(dá)到治療血栓的效果[1]。目前,抗血小板藥物在治療過(guò)程中,很可能抑制正常的止血途徑而引發(fā)出血性
[Abstract]:When the vascular wall is damaged, the human body will initiate hemostatic pathway to protect the damaged blood vessels, but anticoagulant factors are beyond the normal range of regulation, and the substances involved in coagulation will accumulate in the vascular wall, leading to pathological thrombosis. Antiplatelet drugs are a kind of important drugs in the treatment of thrombus. Some key substances or signal pathways in the process of platelet aggregation are used as therapeutic targets to down-regulate the adhesion function of platelet integrin 偽 鈪，

本文編號(hào)：2520119