Document Detail

Microcirculation and venous ulcers: a review.
MedLine Citation:
PMID:  16247708     Owner:  NLM     Status:  MEDLINE    
Recent histological and immunocytochemical analyses of venous leg ulcers suggest that lesions observed in the different stages of chronic venous insufficiency (CVI) may be related to an inflammatory process. This inflammatory process leads to fibrosclerotic remodeling of the skin and then to ulceration. The vascular network of the most superficial layers of the skin appears to be the target of the inflammatory reaction. Hemodynamic forces such as venous hypertension, circulatory stasis, and modified conditions of shear stress appear to play an important role in an inflammatory reaction accompanied by leukocyte activation which clinically leads to CVI: venous dermatitis and venous ulceration. The leukocyte activation is accompanied by the expression of integrins and by synthesis and release of many inflammatory molecules, including proteolytic enzymes, leukotrienes, prostaglandin, bradykinin, free oxygen radicals, cytokines, and possibly other classes of inflammatory mediators. The inflammatory reaction perpetuates itself, leading to liposclerotic skin and subcutaneous tissue remodeling. In light of the mechanisms of venous ulcer formation cited above, therapy in the future might be directed against leukocyte activation in order to diminish the magnitude of the inflammatory response. With this in mind, the attention of many investigators has been drawn to two different drugs with an anti-inflammatory effect: pentoxifylline and flavonoids.
Luigi Pascarella; Geert W Schmid Schönbein; John J Bergan
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Annals of vascular surgery     Volume:  19     ISSN:  0890-5096     ISO Abbreviation:  Ann Vasc Surg     Publication Date:  2005 Nov 
Date Detail:
Created Date:  2005-10-31     Completed Date:  2006-01-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8703941     Medline TA:  Ann Vasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  921-7     Citation Subset:  IM    
Department of Bioengineering, Whitaker Institute of Biomedical Engineering, Jacobs School of Engineering, University of California San Diego, La Jolla, CA, USA.
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MeSH Terms
Endothelium, Vascular / physiopathology
Inflammation Mediators / blood*
Integrin alpha4beta1 / blood
Intercellular Adhesion Molecule-1 / blood
Leukocytes / physiology
Lymphocyte Function-Associated Antigen-1 / blood
Reverse Transcriptase Polymerase Chain Reaction
Varicose Ulcer / physiopathology*
Vascular Cell Adhesion Molecule-1 / blood
Reg. No./Substance:
0/Inflammation Mediators; 0/Integrin alpha4beta1; 0/Lymphocyte Function-Associated Antigen-1; 0/Vascular Cell Adhesion Molecule-1; 126547-89-5/Intercellular Adhesion Molecule-1

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