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Microvascular Permeability
Cellular and Integrative Biology, Division of Biomedical Sciences, Imperial College School of Medicine, London, United Kingdom; and Department of Human Physiology, School of Medicine, University of California, Davis, California Michel, C. C. and F. E. Curry. Microvascular Permeability. Physiol. Rev....
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Published in: | Physiological reviews 1999-07, Vol.79 (3), p.703-761 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Cellular and Integrative Biology, Division of Biomedical Sciences,
Imperial College School of Medicine, London, United Kingdom; and
Department of Human Physiology, School of Medicine, University of
California, Davis, California
Michel, C. C. and
F. E. Curry.
Microvascular Permeability. Physiol. Rev. 79: 703-761, 1999. This review
addresses classical questions concerning microvascular permeabiltiy in
the light of recent experimental work on intact microvascular beds,
single perfused microvessels, and endothelial cell cultures. Analyses,
based on ultrastructural data from serial sections of the clefts
between the endothelial cells of microvessels with continuous walls,
conform to the hypothesis that different permeabilities to water and
small hydrophilic solutes in microvessels of different tissues can be
accounted for by tortuous three-dimensional pathways that pass
through breaks in the junctional strands. A fiber matrix ultrafilter at
the luminal entrance to the clefts is essential if microvascular walls
are to retain their low permeability to macromolecules. Quantitative
estimates of exchange through the channels in the endothelial cell
membranes suggest that these contribute little to the permeability of
most but not all microvessels. The arguments against the convective
transport of macromolecules through porous pathways and for the passage
of macromolecules by transcytosis via mechanisms linked to the
integrity of endothelial vesicles are evaluated. Finally, intracellular
signaling mechanisms implicated in transient increases in venular
microvessel permeability such as occur in acute inflammation are
reviewed in relation to studies of the molecular mechanisms involved in
signal transduction in cultured endothelial cells. |
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ISSN: | 0031-9333 1522-1210 |
DOI: | 10.1152/physrev.1999.79.3.703 |