Effect of lung inflation on active and passive liquid clearance from in vivo rabbit lung

1994 ◽  
Vol 267 (4) ◽  
pp. L482-L487 ◽  
Author(s):  
N. G. Vejlstrup ◽  
C. A. Boyd ◽  
K. L. Dorrington
Keyword(s):  
Sodium Transport ◽  
Left Lung ◽  
Alveolar Epithelium ◽  
Active Sodium ◽  
Rabbit Lung ◽  
Lung Inflation ◽  
Active Sodium Transport ◽  
Active Liquid ◽  
Alveolar Liquid

Active sodium transport contributes to liquid clearance from the alveoli. We hypothesized that the magnitude of active transport of alveolar liquid depends on the extent to which the alveolar epithelium is stretched and, consequently, on the degree of alveolar inflation. In a study on 38 adult rabbits, the left lung was filled in vivo with a solution of glucose (10 mmol/l) made isosmotic with plasma, using sodium chloride, and held at a constant airway pressure of 3, 6, or 9 cmH2O for 6 h. Alveolar liquid clearance was measured directly as a flow into a left main bronchial catheter. Control animals were compared with animals in which active epithelial sodium transport was inhibited by adding amiloride and phloridzin (both 1 mmol/l) to the instillate. At low inflation, active sodium transport reversed a secretion of liquid into the alveoli; at high inflation, active sodium transport made little or no contribution to transepithelial flow. Hydraulic conductance of the left lung was 1.57 microliters.min-1.cmH2O-1.kg body wt-1. The experiments suggest that pulmonary inflation renders active liquid clearance ineffective.

Tight monolayers of rat alveolar epithelial cells: bioelectric properties and active sodium transport

1989 ◽  
Vol 256 (3) ◽  
pp. C688-C693 ◽  
Author(s):  
J. M. Cheek ◽  
K. J. Kim ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Short Circuit ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Active Sodium ◽  
Alveolar Epithelial ◽  
Active Sodium Transport ◽  
Complex Anatomy

Because the pulmonary alveolar epithelium separates air spaces from a fluid-filled compartment, it is expected that this barrier would be highly resistant to the flow of solutes and water. Investigation of alveolar epithelial resistance has been limited due to the complex anatomy of adult mammalian lung. Previous efforts to study isolated alveolar epithelium cultured on porous substrata yielded leaky monolayers. In this study, alveolar epithelial cells isolated from rat lungs and grown on tissue culture-treated Nucleopore filters resulted in tight monolayers with transepithelial resistance greater than 2,000 omega.cm2. Changes in bioelectric properties of these alveolar epithelial monolayers in response to ouabain, amiloride, and terbutaline are consistent with active sodium transport across a polarized barrier. 22Na flux measurements under short-circuit conditions directly confirm net transepithelial absorption of sodium by alveolar epithelial cells in the apical to basolateral direction, comparable to the observed short-circuit current (4.37 microA/cm2). The transport properties of these tight monolayers may be representative of the characteristics of the mammalian alveolar epithelial barrier in vivo.

Increase of lung sodium-potassium-ATPase activity during recovery from high-permeability pulmonary edema

1996 ◽  
Vol 271 (6) ◽  
pp. L896-L909 ◽  
Author(s):  
D. Zuege ◽  
S. Suzuki ◽  
Y. Berthiaume
Keyword(s):  
Atpase Activity ◽  
Pulmonary Edema ◽  
Sodium Transport ◽  
Sodium Ion ◽  
Type Ii ◽  
Active Sodium ◽  
Sodium Potassium ◽  
Sodium Ion Transport ◽  
Active Sodium Transport

Previous studies have suggested that recovery from pulmonary edema may be dependent on active sodium ion transport. Most of the data supporting this concept came from work done in isolated type II cells, isolated lung preparations, or in models of alveolar flooding. There is a limited amount of information regarding the role of active sodium ion transport in vivo. Furthermore, most of this information was obtained in one model of pulmonary edema, the hyperoxic lung injury model. The purpose of these experiments was then to measure the activity of the sodium-potassium-adenosinetriphosphatase (Na(+)-K(+)-ATPase), the active component of the sodium transport process and an indirect marker of active sodium transport, during recovery from thiourea-induced pulmonary edema in rats. Na(+)-K(+)-ATPase activity was significantly increased during recovery from lung edema. This increase could not be accounted for by the Na(+)-K(+)-ATPase activity present in inflammatory cells recruited in the lung by the injury process or by a direct impact of thiourea on the enzyme. Alveolar flooding, induced by instillation of a protein-containing solution into the airways of ventilated rats also increased the activity of Na(+)-K(+)-ATPase, suggesting that activation of the enzyme is probably secondary to either the presence of edema or the physiological consequences associated with edema. The quantity of lung Na(+)-K(+)-ATPase protein was also elevated during edema resolution, indicating that augmented synthesis of this enzyme underlies the increased enzyme activity observed. The quantity of Na(+)-K(+)-ATPase protein in alveolar type II cells was also significantly enhanced during recovery from edema, suggesting that these cells contribute to active sodium transport in vivo. The results of this study suggest that active sodium transport could participate in the resolution of pulmonary edema.

Evidence for active sodium transport across alveolar epithelium of isolated rat lung

1987 ◽  
Vol 62 (6) ◽  
pp. 2460-2466 ◽  
Author(s):  
B. E. Goodman ◽  
K. J. Kim ◽  
E. D. Crandall
Keyword(s):  
Sodium Transport ◽  
Alveolar Epithelial Cell ◽  
Control Period ◽  
Alveolar Epithelium ◽  
Rat Lung ◽  
Alveolar Space ◽  
Active Sodium ◽  
Apparent Permeability ◽  
Lung Weight ◽  
Active Sodium Transport

We have previously presented evidence that cultured alveolar epithelial cell monolayers actively transport sodium from medium to substratum, a process that can be inhibited by sodium transport blockers and stimulated by beta-agonists. In this study, the isolated perfused rat lung was utilized in order to investigate the presence of active sodium transport by intact adult mammalian alveolar epithelium. Radioactive tracers (22Na and [14C]sucrose) were instilled into the airways of isolated Ringer-perfused rat lungs whose weight was continuously monitored. The appearance of isotopes in the recirculated perfusate was measured, and fluxes and apparent permeability-surface area products were determined. A pharmacological agent (amiloride, ouabain, or terbutaline) was added to the perfusate during each experiment after a suitable control period. Amiloride and ouabain resulted in decreased 22Na fluxes and a faster rate of lung weight gain. Terbutaline resulted in increased 22Na flux and a more rapid rate of lung weight loss. [14C]sucrose fluxes were unchanged by the presence of these pharmacological agents. These data are most consistent with the presence of a regulable active component of sodium transport across intact mammalian alveolar epithelium that leads to removal of sodium from the alveolar space, with anions and water following passively. Regulation of the rate of sodium and fluid removal from the alveolar space may play an important role in the prevention and/or resolution of alveolar pulmonary edema.

Evidence for regulation of sodium transport from airspace to vascular space by cAMP

1989 ◽  
Vol 257 (2) ◽  
pp. L86-L93 ◽  
Author(s):  
B. E. Goodman ◽  
J. L. Anderson ◽  
J. W. Clemens
Keyword(s):  
Sodium Transport ◽  
Phosphodiesterase Inhibitor ◽  
Alveolar Epithelium ◽  
Active Sodium ◽  
Apparent Permeability ◽  
Fluid Removal ◽  
Active Sodium Transport ◽  
Vascular Space ◽  
Camp Analogue ◽  
Permeability Surface

Evidence has been accumulating that regulation of the rate of solute and fluid removal from the alveolar spaces may play an important role in the prevention and/or resolution of alveolar pulmonary edema. In this study, the isolated perfused rat lung was used to investigate the effects of an adenosine 3',5'-cyclic monophosphate (cAMP) analogue or a phosphodiesterase inhibitor on active sodium transport from airspace to vascular space. Three tracers were instilled into the airways of isolated Krebs-Ringer bicarbonate solution (KRB)-perfused rat lungs. The appearance of tracers in the single-pass perfusate was measured, and the apparent permeability-surface area products (PS) were calculated for each tracer at each sample time based on Fick's first law of diffusion. After steady-state PS values had been reached, a cAMP analogue or phosphodiesterase inhibitor was added to the perfusate. Both agents caused significant increases in the PS for 22Na. In another group of experiments, a cAMP analogue was added to the perfusate, followed by the subsequent addition of a sodium transport inhibitor and the resultant large decrease in the PS for 22Na. These data are consistent with the regulation of active sodium transport across the intact mammalian alveolar epithelium by a cAMP-mediated process leading to removal of sodium from the alveolar spaces, with anions and water following passively.

Sign in / Sign up

Export Citation Format

Share Document