Source:http://linkedlifedata.com/resource/pubmed/id/17950075
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2007-10-22
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pubmed:abstractText |
In acute respiratory distress syndrome, pulmonary vascular permeability increases, causing intravascular fluid and protein to move into the lung's interstitium. The classic model describing the formation of pulmonary edema suggests that fluid crossing the capillary endothelium is drawn by negative interstitial pressure into the potential space surrounding extra-alveolar vessels and, as interstitial pressure builds, is forced into the alveolar air space. However, the validity of this model is challenged by animal models of acute lung injury in which extra-alveolar vessels are more permeable than capillaries under a variety of conditions. In the current study, we sought to determine whether extravascular fluid accumulation can be produced because of increased permeability of either the capillary or extra-alveolar endothelium, and whether different pathophysiology results from such site-specific increases in permeability.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carcinogens,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Phorbol Esters,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin,
http://linkedlifedata.com/resource/pubmed/chemical/phorbol-12,13-didecanoate
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-4804
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
143
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
70-7
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pubmed:meshHeading |
pubmed-meshheading:17950075-Animals,
pubmed-meshheading:17950075-Carcinogens,
pubmed-meshheading:17950075-Cell Membrane Permeability,
pubmed-meshheading:17950075-Disease Models, Animal,
pubmed-meshheading:17950075-Endothelial Cells,
pubmed-meshheading:17950075-Enzyme Inhibitors,
pubmed-meshheading:17950075-Extravascular Lung Water,
pubmed-meshheading:17950075-Lung,
pubmed-meshheading:17950075-Lung Compliance,
pubmed-meshheading:17950075-Male,
pubmed-meshheading:17950075-Phorbol Esters,
pubmed-meshheading:17950075-Pulmonary Alveoli,
pubmed-meshheading:17950075-Pulmonary Edema,
pubmed-meshheading:17950075-Rats,
pubmed-meshheading:17950075-Rats, Sprague-Dawley,
pubmed-meshheading:17950075-Respiratory Distress Syndrome, Adult,
pubmed-meshheading:17950075-Respiratory Mechanics,
pubmed-meshheading:17950075-Thapsigargin
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pubmed:year |
2007
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pubmed:articleTitle |
Phenotypic heterogeneity in lung capillary and extra-alveolar endothelial cells. Increased extra-alveolar endothelial permeability is sufficient to decrease compliance.
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pubmed:affiliation |
Center for Lung Biology, University of South Alabama College of Medicine, Mobile, Alabama 36688, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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