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创伤与器官功能障碍中的组织因子。

Tissue factor in trauma and organ dysfunction.

作者信息

Gando Satoshi

机构信息

Division of Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

出版信息

Semin Thromb Hemost. 2006 Feb;32(1):48-53. doi: 10.1055/s-2006-933340.

Abstract

Tissue factor (TF) performs an essential role in the blood clotting system by activating the extrinsic coagulation pathway following vascular injury. In addition to this physiological hemostatic role for wound repair, TF also plays pivotal roles in organ dysfunction in trauma patients by triggering pathological disseminated thrombosis and inflammation. Constitutively expressed TF in subendothelial cells is released into the circulation following trauma and can be detected as slightly elevated TF levels in the plasma. Liberation of constitutive TF into the blood and inducible tissue factor expression on monocytes and the other cells may synergistically increase plasma TF levels to higher values at the early stage of posttrauma, especially in patients with disseminated intravascular coagulation (DIC) in association with sustained systemic inflammatory response syndrome. Marked TF generation not adequately balanced by physiological coagulation inhibitors such as tissue factor pathway inhibitor in posttrauma DIC patients has been observed. Based on these pieces of evidence, it has now been accepted that combined activation of TF-dependent coagulation inadequately regulated by anticoagulant mechanisms and inflammation may synergistically play important roles in the pathogenesis of posttrauma multiple organ dysfunction syndrome.

摘要

组织因子(TF)通过在血管损伤后激活外源性凝血途径,在血液凝固系统中发挥重要作用。除了在伤口修复中的这种生理性止血作用外,TF还通过引发病理性弥散性血栓形成和炎症,在创伤患者的器官功能障碍中起关键作用。创伤后,内皮下细胞中组成性表达的TF释放到循环中,血浆中TF水平可检测到略有升高。组成性TF释放到血液中以及单核细胞和其他细胞上诱导性组织因子表达,可能在创伤后早期协同将血浆TF水平提高到更高值,尤其是在伴有持续性全身炎症反应综合征的弥散性血管内凝血(DIC)患者中。在创伤后DIC患者中,已观察到由组织因子途径抑制物等生理性凝血抑制剂无法充分平衡的显著TF生成。基于这些证据,目前已公认,由抗凝机制调节不足的TF依赖性凝血与炎症的联合激活可能在创伤后多器官功能障碍综合征的发病机制中协同发挥重要作用。

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