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Microvascular permeability, venous stasis and oedema.

Authors: C C, Michel;

Microvascular permeability, venous stasis and oedema.

Abstract

Microvascular permeability to fluid and hydrophilic solutes is restricted to channels between the endothelial cells and through the fenestrations when these are present. The channels have a molecular filter which appears to be a lattice of fibrous molecules reinforced by plasma proteins. The quantitative description of blood-tissue fluid movements is complicated by plasma protein permeation which leads to a non-linear steady state relation between fluid filtration and microvascular pressure. When fluid filtration is low it can be balanced by lymph flow but at high pressures oedema develops. Microvascular pressure rises less than expected with increments of venous pressure owing to local vasoconstriction of the arterioles. The sluggish flow which results from this vasoconstriction and high venous pressure leads to a haemoconcentration which reduces oedema formation but favours leucocyte and platelet sequestration within the microcirculation.

Related Organizations
Keywords

Capillary Permeability, Venous Insufficiency, Vasoconstriction, Animals, Edema, Humans

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average
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