| Hydraulic conductance of pulmonary microvascular and macrovascular endothelial cell monolayers. | |
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MedLine Citation:
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PMID: 16760315 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Endothelial cells isolated from pulmonary arteries (RPAEC) and microcirculation (RPMVEC) of rat lungs were grown to confluence on porous filters and mounted on an Ussing-type chamber. Transmembrane pressure (deltaP) was controlled by the reservoir height, and the filtration rate corrected for surface area (J(v)/A) was measured by timing fluid movement in a calibrated micropipette. These parameters were used to calculate hydraulic conductance (Lp) by using linear regression of J(v)/A on deltaP. Mean Lp values for newly confluent RPAEC monolayers were 22 times higher than those for RPMVEC monolayers (28.6 +/- 5.6 vs. 1.30 +/- 0.50 x 10(-7) cm x s(-1) x cmH2O(-1); P < or = 0.01). After confluence was reached, electrical resistance and Lp remained stable in RPAEC but continued to change in RPMVEC with days in culture. Both phenotypes exhibited an initial time-dependent sealing response, but Lp also had an inverse relationship to deltaP in RPMVEC monolayers > or = 4 days postconfluence that was attributed to cell overgrowth rather than junctional length. In a comparison of the cadherin contents, E-cadherin was predominant in RPMVEC, but VE-cadherin was predominant in RPAEC. At a constant deltaP of 40-45 cmH2O for 2 h, J(v)/A increased 225% in RPAEC monolayers but did not change significantly in RPMVEC monolayers. Significant decreases in Lp were obtained after treatment with 5% albumin, GdCl3, or isoproterenol plus rolipram in both phenotypes. Thus lung microvascular endothelial cells exhibited a significantly lower Lp than conduit vessel endothelium, which would limit alveolar flooding relative to perivascular edema cuff formation during increased pulmonary vascular pressures. |
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Authors:
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James C Parker; Troy Stevens; Jason Randall; David S Weber; Judy A King |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 291 ISSN: 1040-0605 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2006 Jul |
Date Detail:
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Created Date: 2006-06-08 Completed Date: 2006-07-25 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L30-7 Citation Subset: IM |
Affiliation:
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Dept. of Physiology, MSB 3074, College of Medicine, Univ. of South Alabama, Mobile, AL 36688, USA. Jparker@usouthal.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic beta-Agonists
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pharmacology Albumins / pharmacology Animals Antigens, CD Cadherins / metabolism Capillary Permeability / drug effects, physiology* Cells, Cultured Endothelial Cells / metabolism*, ultrastructure Endothelium, Vascular / cytology, metabolism* Filtration Gadolinium / pharmacology Gap Junctions / metabolism, ultrastructure Isoproterenol / pharmacology Lung / blood supply* Microscopy, Electron Phosphodiesterase Inhibitors / pharmacology Pressure Pulmonary Edema / metabolism* Rats Rats, Sprague-Dawley Rolipram / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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P01 HL-66299/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Agonists; 0/Albumins; 0/Antigens, CD; 0/Cadherins; 0/Phosphodiesterase Inhibitors; 0/cadherin 5; 61413-54-5/Rolipram; 7440-54-2/Gadolinium; 7683-59-2/Isoproterenol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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