Carson S D, Johnson D R, Tracy S M
University of Nebraska Medical Center, Department of Pathology and Microbiology, Omaha 68198-6495.
Eur Heart J. 1993 Dec;14 Suppl K:98-104.
Tissue factor is a potent initiator of blood coagulation. In tissue sections, it has been immunologically demonstrated in cells normally not in contact with circulating blood, and elevated activity has been repeatedly demonstrated in peripheral blood monocytes of patients considered to be at risk for thrombosis. Studies with endothelial cells and monocytes in culture have documented the induction of tissue factor synthesis by biochemical mediators of the inflammatory process. Lytic processes, such as those caused by complement activation or viral infections, increase the tissue factor activity several fold over the basal level of the affected cells. Diminished anti-thrombotic properties of endothelium, and induced tissue factor expression in endothelium and monocytes/macrophages, combined with the increased specific procoagulant activity resulting from cell membrane damage, may endow inflammatory foci with dramatically elevated procoagulant activity. Levels of tissue factor activity at which procoagulant mechanisms escape regulation by natural anticoagulant mechanisms and produce thrombosis remain to be determined.
组织因子是血液凝固的强效启动因子。在组织切片中,已通过免疫方法在通常不与循环血液接触的细胞中证实了其存在,并且在被认为有血栓形成风险的患者的外周血单核细胞中反复证实其活性升高。对培养的内皮细胞和单核细胞的研究记录了炎症过程的生化介质对组织因子合成的诱导作用。诸如补体激活或病毒感染所引起的溶解过程,会使受影响细胞的组织因子活性比基础水平增加几倍。内皮细胞抗血栓特性的减弱,以及在内皮细胞和单核细胞/巨噬细胞中诱导的组织因子表达,再加上细胞膜损伤导致的特定促凝活性增加,可能会使炎症灶具有显著升高的促凝活性。促凝机制逃避天然抗凝机制的调节并产生血栓形成的组织因子活性水平仍有待确定。