Mackie I J, Bull H A
Haematology Department, Middlesex Hospital, London, UK.
Blood Rev. 1989 Dec;3(4):237-50. doi: 10.1016/0268-960x(89)90031-3.
Regulation of normal haemostasis and blood flow involves complex interactions between plasma proteins and blood cells, including platelets, leukocytes and the endothelial lining of blood vessels. Thrombin acts as a pivot in the maintenance of the haemostatic balance; the vascular endothelial cell in particular limits the generation of thrombin by localisation of anticoagulant processes on its luminal membrane. The endothelial cell synthesises key molecules in this process and also binds exogenously derived molecules, as well as releasing proteins of the fibrinolysis cascade. The thromboresistance of the luminal surface is further regulated by lipoxygenase and cyclo-oxygenase metabolites of unsaturated fatty acids synthesised by the endothelial cell. In response to trauma, inflammatory reactions, normal wound healing and in association with a variety of disease states, the anticoagulant and fibrinolytic mechanisms are downregulated and the procoagulant and thrombotic mechanisms predominate with resultant generation of thrombin, fibrin clot formation and subsequent platelet adhesion and aggregation. Pro-inflammatory and prothrombotic cytokines downregulate the fibrinolytic and activated protein C pathways as well as inducing synthesis of specific procoagulant and prothrombotic mediators by platelets and leukocytes as well as endothelium.
正常止血和血流调节涉及血浆蛋白与血细胞（包括血小板、白细胞和血管内皮）之间的复杂相互作用。凝血酶在维持止血平衡中起关键作用；特别是血管内皮细胞通过在其腔面膜上定位抗凝过程来限制凝血酶的产生。内皮细胞在这一过程中合成关键分子，还能结合外源性分子，并释放纤维蛋白溶解级联反应的蛋白质。内皮细胞合成的不饱和脂肪酸的脂氧合酶和环氧化酶代谢产物进一步调节腔表面的抗血栓形成能力。在创伤、炎症反应、正常伤口愈合以及与多种疾病状态相关的情况下，抗凝和纤维蛋白溶解机制下调，促凝和血栓形成机制占主导，导致凝血酶生成、纤维蛋白凝块形成以及随后的血小板黏附和聚集。促炎和促血栓形成细胞因子下调纤维蛋白溶解和活化蛋白C途径，同时诱导血小板、白细胞以及内皮细胞合成特定的促凝和促血栓形成介质。
