Venous Valvular Stasis-Associated Hypoxia and Thrombosis: What Is the Link?

被引：136

作者：

Bovill, Edwin G. ^{[1
]}

van der Vliet, Albert ^{[1
]}

机构：

[1] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT 05405 USA

来源：

ANNUAL REVIEW OF PHYSIOLOGY, VOL 73 | 2011年 / 73卷

关键词：

venous thrombosis; tissue factor; microvesicle; hypoxia-inducible factor-1 (HIF-1); P-selectin; endothelium; TISSUE FACTOR EXPRESSION; HUMAN-ENDOTHELIAL-CELLS; SMALL-MOLECULE INHIBITOR; DEEP-VEIN THROMBOSIS; P-SELECTIN PSI-697; NF-KAPPA-B; PULMONARY-EMBOLISM; RISK-FACTORS; SUBCLINICAL ATHEROSCLEROSIS; PROCOAGULANT ACTIVITY;

D O I：

10.1146/annurev-physiol-012110-142305

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

This review focuses on the role of the venous valves in the genesis of thrombus formation in venous thromboembolic disease (VTE). Clinical VTE and the evidence for the valvular origin of venous thrombosis are reviewed. Virchow's triad is then used as a framework for discussion to approach the question posed regarding the link between venous valvular stasis associated hypoxia and thrombosis. Thus, the effects of blood flow stasis, hypercoagulability of blood, and the characteristics of the vessel wall within the venous valvular sinus are assessed in turn.

引用

页码：527 / 545

页数：19

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