Document Detail

Transcapillary exchange: role and importance of the interstitial fluid pressure and the extracellular matrix.
MedLine Citation:
PMID:  20472565     Owner:  NLM     Status:  MEDLINE    
This review will summarize current knowledge on the role of the extracellular matrix (ECM) in general and on the interstitial fluid pressure (P(if)) in particular with regard to their importance in transcapillary exchange. The fluid volume in the interstitial space is normally regulated within narrow limits by automatic re-adjustment of the interstitial hydrostatic and colloid osmotic pressures in response to perturbations in capillary filtration and by the lymphatics. Contrary to this commonly accepted view, P(if) can become an active force and create a fluid flux across the capillaries in several inflammatory reactions and trauma situations rather than limit the changes occurring. The molecular mechanisms involved in the lowering of P(if) include the release of cellular tension exerted on the collagen and microfibril networks in the connective tissue via the collagen-binding beta(1)-integrins, thereby allowing the glycosaminoglycan ground substance, which is normally underhydrated, to expand and take up fluid. Several growth factors and cytokines, including the platelet-derived growth factor BB, are able to reverse a lowering of P(if) and restore the normal compaction of the ECM. The magnitude of the lowering of P(if) varies with the inflammatory response. In several inflammatory reactions, a lowering of P(if) to -5 to -10 mmHg is seen, which will increase capillary filtration by 10-20 times since the normal capillary filtration pressure is usually 0.5-1 mmHg (skin and skeletal muscle). Unless this lowering of P(if) is taken into account, the enhanced solute flux resulting from an inflammatory response will be ascribed to an increased capillary permeability.
Rolf K Reed; Kristofer Rubin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-05-13
Journal Detail:
Title:  Cardiovascular research     Volume:  87     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-02     Completed Date:  2010-10-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  211-7     Citation Subset:  IM    
Department of Biomedicine, University of Bergen, Jonas Lies vei 91, Bergen, Norway.
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MeSH Terms
Antigens, CD29 / metabolism
Body Fluids / metabolism*
Capillaries / immunology,  metabolism*,  physiopathology
Capillary Permeability*
Cytoskeleton / metabolism
Edema / metabolism,  physiopathology
Endothelium, Vascular / immunology,  metabolism*,  physiopathology
Extracellular Fluid / metabolism*
Extracellular Matrix / metabolism*
Hydrostatic Pressure
Inflammation / metabolism,  physiopathology
Inflammation Mediators / metabolism
Integrin alpha2beta1 / metabolism
Models, Cardiovascular
Osmotic Pressure
Signal Transduction
Reg. No./Substance:
0/Antigens, CD29; 0/Inflammation Mediators; 0/Integrin alpha2beta1

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