止血是一种生理反应，可在受伤船舶中排放出血的生理反应。在正常情况下，血管内皮促血管抑制，抑制血小板粘附和活化，抑制凝固，增强纤维蛋白切割，是抗炎性的。在急性血管创伤下，血管收缩机制占主导地位，内皮细胞变为孕激素，促血糖和促炎本质上。这是通过减少内皮扩张剂的减少来实现：腺苷，不和前列腺素;通过ADP，Serotonin和血栓乳糖对血管平滑肌细胞的直接作用引发他们的收缩（Becker等，2000）。导致形成止血血栓形成的内皮函数变化的主要触发是血液和细胞外基质组分之间的内皮细胞势垒（Ruggeri 2002）的丧失。循环血小板识别和区分内皮病变的区域;在这里，它们坚持暴露的亚内皮。它们与各种血栓形成底物和局部产生或释放的激动剂的相互作用导致血小板活化。该方法被描述为具有两个阶段，首先，粘附 - 表面上的初始束缚，其次聚集 - 血小板血小板内聚力（野蛮和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.