Esmon C T
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA.
J Thromb Haemost. 2003 Jul;1(7):1343-8. doi: 10.1046/j.1538-7836.2003.00261.x.
Systemic inflammation is a potent prothrombotic stimulus. Inflammatory mechanisms upregulate procoagulant factors, downregulate natural anticoagulants and inhibit fibrinolytic activity. In addition to modulating plasma coagulation mechanisms, inflammatory mediators appear to increase platelet reactivity. In vivo, however, natural anticoagulants not only prevent thrombosis, but they also dampen inflammatory activity. Some insights into the evolution and linkages between inflammatory mechanisms and the coagulation/anticoagulation mechanisms have become evident from recent structural studies. This review will summarize the interactions between inflammation and coagulation.
全身炎症是一种强大的促血栓形成刺激因素。炎症机制上调促凝血因子,下调天然抗凝剂并抑制纤维蛋白溶解活性。除了调节血浆凝血机制外,炎症介质似乎还会增加血小板反应性。然而,在体内,天然抗凝剂不仅可预防血栓形成,还能抑制炎症活动。最近的结构研究已经揭示了一些关于炎症机制与凝血/抗凝机制之间的演变及联系的见解。本综述将总结炎症与凝血之间的相互作用。