Document Detail


Hydraulic conductance of pulmonary microvascular and macrovascular endothelial cell monolayers.
MedLine Citation:
PMID:  16760315     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
James C Parker; Troy Stevens; Jason Randall; David S Weber; Judy A King
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
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:
Created Date:  2006-06-08     Completed Date:  2006-07-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L30-7     Citation Subset:  IM    
Affiliation:
Dept. of Physiology, MSB 3074, College of Medicine, Univ. of South Alabama, Mobile, AL 36688, USA. Jparker@usouthal.edu
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / 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:
P01 HL-66299/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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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