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Am J Physiol Lung Cell Mol Physiol 292: L378-L380, 2007. First published October 13, 2006; doi:10.1152/ajplung.00196.2006
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PERSPECTIVES

Hydraulic conductance of lung endothelial phenotypes and Starling safety factors against edema

James C. Parker

Department of Physiology, Center for Lung Biology, College of Medicine, University of South Alabama, Mobile, Alabama

ABSTRACT

Recent permeability studies comparing endothelial cell phenotypes derived from alveolar and extra-alveolar vessels have significant implications for interpreting the mechanisms of fluid homeostasis in the intact lung. These studies indicate that confluent monolayers of rat pulmonary microvascular endothelial cells had a hydraulic conductance (Lp) that was only 5% and a transendothelial flux rate for 72-kDa dextran only 9% of values determined for rat pulmonary artery endothelial cell monolayers. On the basis of previous studies partitioning the filtration coefficients between alveolar and extra-alveolar vascular segments in rat lungs and previous studies of lymph albumin fluxes and permeability, the contribution of the alveolar capillary segment to total albumin flux in lymph was estimated to be less than 10%. In addition, the Starling safety factors against the edema calculated for the alveolar capillaries are quite different from those estimated for whole lung. Estimates of the edema safety factor due to increased filtration across the alveolar capillary wall based on the low Lp indicate it is quantitatively the greatest safety factor, although it would be a minor safety factor for extra-alveolar vessels. Also, a markedly higher effective protein osmotic absorptive force for plasma proteins must occur in the capillaries relative to extra-alveolar vessels. The lower Lp for alveolar capillaries also has implications for the sequence of hydrostatic edema formation, and it also may have a role in preventing exercise-induced alveolar flooding.

capillary permeability; pulmonary edema; lymph flow



Address for reprint requests and other correspondence: J. C. Parker, Dept. of Physiology, College of Medicine, Univ. of South Alabama, 307 University Blvd., Mobile, AL 36688 (jparker{at}usouthal.edu)




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