Document Detail


Venous valvular stasis-associated hypoxia and thrombosis: what is the link?
MedLine Citation:
PMID:  21034220     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Edwin G Bovill; Albert van der Vliet
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Annual review of physiology     Volume:  73     ISSN:  1545-1585     ISO Abbreviation:  Annu. Rev. Physiol.     Publication Date:  2011  
Date Detail:
Created Date:  2011-02-14     Completed Date:  2011-07-08     Revised Date:  2012-03-22    
Medline Journal Info:
Nlm Unique ID:  0370600     Medline TA:  Annu Rev Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  527-45     Citation Subset:  IM    
Affiliation:
Department of Pathology, University of Vermont College of Medicine, Burlington, 05405, USA. edwin.bovill@uvm.edu
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MeSH Terms
Descriptor/Qualifier:
Aging / physiology
Anoxia / physiopathology*
Blood Coagulation / physiology
Early Growth Response Protein 1 / physiology
Female
Humans
Hypoxia-Inducible Factor 1 / physiology
Male
Reactive Oxygen Species / metabolism
Thrombosis / epidemiology,  physiopathology*
Veins / physiopathology
Venous Valves / physiopathology*
Grant Support
ID/Acronym/Agency:
P01 HL046703/HL/NHLBI NIH HHS; R01 HL085646/HL/NHLBI NIH HHS; R01 HL085646-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/EGR1 protein, human; 0/Early Growth Response Protein 1; 0/Hypoxia-Inducible Factor 1; 0/Reactive Oxygen Species

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