止血是一种生理反应，在受伤血管出血停止时达到高潮。正常情况下，血管内皮支持血管扩张，抑制血小板粘附和活化，抑制凝血，增强纤维蛋白分裂，具有抗炎作用。在急性血管创伤下，血管收缩机制占优势，内皮在本质上成为血栓前、促凝和促炎。这是通过减少内皮扩张剂:腺苷、NO和前列环素;并通过ADP、血清素和血栓素对血管平滑肌细胞的直接作用引起它们的收缩(Becker et al. 2000)。导致凝血血栓形成的内皮功能变化的主要触发因素是血液和细胞外基质成分之间内皮细胞屏障的丧失(Ruggeri 2002)。循环血小板识别和区分内皮病变区域;这里，它们附着在暴露的内皮下层。它们与各种血栓形成底物和局部生成或释放的激动剂相互作用，导致血小板激活。这个过程被描述为有两个阶段，第一阶段是粘附-最初附着在表面上，第二阶段是聚集-血小板-血小板内聚(Savage和Cattaneo等，2001)。 Three mechansism contribute to the loss of blood following vessel injury. The vessel constricts, reducing the loss of blood. Platelets adhere to the site of injury, become activated and aggregate with fibrinogen into a soft plug that limits blood loss, a process termed primary hemostasis. Proteins and small molecules are released from granules by activated platelets, stimulating the plug formation process. Fibrinogen from plasma forms bridges between activated platelets. These events initiate the clotting cascade (secondary hemostasis). Negatively-charged phospholipids exposed at the site of injury and on activated platelets interact with tissue factor, leading to a cascade of reactions that culminates with the formation of an insoluble fibrin clot.