Lung inflation, lung solute permeability, and alveolar edema

1982 ◽  
Vol 53 (1) ◽  
pp. 121-125 ◽  
Author(s):  
E. A. Egan
Keyword(s):  
Alveolar Space ◽  
Lung Epithelium ◽  
Lung Inflation ◽  
Solute Permeability ◽  
Entire Lung ◽  
Series Of Experiments ◽  
Gas Volume ◽  
Protein Permeability ◽  
Alveolar Edema ◽  
Alveolar Liquid

A series of experiments in anesthetized rabbits were conducted to determine whether hyperinflation of the lung alone could produce a protein-permeable lung epithelium and whether a protein-permeable lung epithelium allowed accumulation of liquid in the alveolar space. Some animals had their entire lungs subjected to distending pressures; others had only an area of the lung subjected to the high distending pressure. Alveolar liquid was measured by dilution of radioactive solutes upon instillation of saline into atelectatic lung, and protein permeability was determined by the loss of labeled albumin from the alveolar space over 40–60 min. Inflation of the entire lung at 40 cmH2O for 20 min increases air-space gas volume three- to fourfold, does not produce a protein-permeable epithelium, and does not result in accumulation of alveolar liquid. Distension of a small area of the lung by 40 cmH2O pressure for 20 min increases the gas volume 6- to 12-fold and produces a protein-permeable epithelium, but does not result in liquid accumulation in the alveoli. It is concluded that only very high distending volumes cause the lung epithelium to become permeable to protein and that a protein-permeable epithelium alone does not induce alveolar edema.

Solute permeability of the alveolar epithelium in acute hemodynamic pulmonary edema in dogs

1977 ◽  
Vol 233 (1) ◽  
pp. H80-H86 ◽  
Author(s):  
E. A. Egan ◽  
R. M. Nelson ◽  
I. H. Gessner
Keyword(s):  
Pulmonary Edema ◽  
Isotonic Saline ◽  
Alveolar Epithelium ◽  
Lung Epithelium ◽  
Solute Permeability ◽  
Blue Dextran ◽  
Lung Segment ◽  
Anesthetized Dogs ◽  
The One ◽  
Alveolar Edema

Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.

Gas transport during high-frequency ventilation

1983 ◽  
Vol 55 (2) ◽  
pp. 472-478 ◽  
Author(s):  
V. Brusasco ◽  
T. J. Knopp ◽  
K. Rehder
Keyword(s):  
Stroke Volume ◽  
Dead Space ◽  
High Frequency ◽  
Oscillation Frequency ◽  
High Frequency Ventilation ◽  
Dead Space Volume ◽  
Entire Lung ◽  
Frequency Ventilation ◽  
Gas Volume ◽  
Space Volume

During high-frequency small-volume ventilation (HFV), the transport rate of gas from the mouth to a lung region is a function of two conductances (conductance is the transfer rate of a gas divided by its partial pressure difference): regional longitudinal gas conductance along the airways (Grlongi) and gas conductance between lung regions (Ginter). Grlongi per unit regional lung (gas) volume [Grlongi/(Vr beta g)] was determined during HFV in 11 anesthetized paralyzed dogs lying supine. The distribution of Grlongi/(Vr beta g) was nearly uniform during HFV when stroke volumes were less than approximately two-thirds of the Fowler dead-space volume. By contrast, the distribution of Grlongi/(Vr beta g) was nonuniform when the stroke volume exceeded approximately two-thirds of the Fowler dead-space volume and the oscillation frequency was 5 Hz. Gas conductance along the airways per unit lung gas volume [average Glongi/(V beta g)], for the entire lung, increased with stroke volume at all frequencies, but for a given product of oscillation frequency and stroke volume, the average Glongi/(V beta g) was greater when stroke volume was large and oscillation frequency was low. The average Glongi/(V beta g) increased with frequency up to a maximal value; the frequency at which the maximum occurred depended on the kinematic viscosity of the inspired gas mixture.

Response of alveolar epithelial solute permeability to changes in lung inflation

1980 ◽  
Vol 49 (6) ◽  
pp. 1032-1036 ◽  
Author(s):  
E. A. Egan
Keyword(s):  
Pore Radius ◽  
Alveolar Epithelium ◽  
Molecular Size ◽  
High Volume ◽  
Lung Inflation ◽  
Solute Permeability ◽  
Alveolar Epithelial ◽  
The Difference ◽  
Total Capacity ◽  
Inflation Volume

The relation between the solute permeability of th alveolar epithelium, characterized as a pore radius, and lung inflation was studied in anesthetized dogs. Pore radius was calculated from measurements of the rate of efflux of several radiolabeled solutes of known molecular size from alveolar saline. Individual animals were studied at two or more separate inflation volumes. The pore radius during the first volume studied averaged 20 A in high-volume animals (mean inflation 82% of capacity) and 15 A at lower volume (mean inflation, 47% of capacity). The difference was significantly P < 0.05. Lungs inflated to total capacity showed free solute movement across the lung epithelium. Increasing inflation volume in an animal always produced a larger pore radius. Decreasing the inflation volume did not produce a smaller pore radius; it remained the same or became larger. Volume induced increases in lung epithelial solute permeability do not reverse immediately at lower volumes, suggesting this phenomenon represents lung injury.

scholarly journals Morphometric changes in the human pulmonary acinus during inflation

2012 ◽  
Vol 112 (6) ◽  
pp. 937-943 ◽  
Author(s):  
A. J. Hajari ◽  
D. A. Yablonskiy ◽  
A. L. Sukstanskii ◽  
J. D. Quirk ◽  
M. S. Conradi ◽  
...  
Keyword(s):  
Human Subjects ◽  
Alveolar Volume ◽  
Healthy Human ◽  
Lung Inflation ◽  
Pulmonary Acinus ◽  
Anisotropic Expansion ◽  
Healthy Human Subjects ◽  
Alveolar Duct ◽  
Gas Volume

Despite decades of research into the mechanisms of lung inflation and deflation, there is little consensus about whether lung inflation occurs due to the recruitment of new alveoli or by changes in the size and/or shape of alveoli and alveolar ducts. In this study we use in vivo 3He lung morphometry via MRI to measure the average alveolar depth and alveolar duct radius at three levels of inspiration in five healthy human subjects and calculate the average alveolar volume, surface area, and the total number of alveoli at each level of inflation. Our results indicate that during a 143 ± 18% increase in lung gas volume, the average alveolar depth decreases 21 ±5%, the average alveolar duct radius increases 7 ± 3%, and the total number of alveoli increases by 96 ± 9% (results are means ± SD between subjects; P < 0.001, P < 0.01, and P < 0.00001, respectively, via paired t-tests). Thus our results indicate that in healthy human subjects the lung inflates primarily by alveolar recruitment and, to a lesser extent, by anisotropic expansion of alveolar ducts.

Massive postmortem bronchoconstriction in guinea pig lungs

1984 ◽  
Vol 56 (2) ◽  
pp. 308-314 ◽  
Author(s):  
Y. L. Lai ◽  
W. J. Lamm ◽  
D. L. Luchtel ◽  
J. Hildebrandt
Keyword(s):  
Guinea Pig ◽  
Airway Obstruction ◽  
Latent Period ◽  
Lung Tissue ◽  
Inflation Pressure ◽  
Lung Inflation ◽  
High Inflation ◽  
Trapped Gas ◽  
Gas Volume

A special phenomenon (difficult to inflate and deflate) occurring in the postmortem guinea pig lungs was studied in 40 animals. Thirty minutes after excision of the lungs or exsanguination, less than 50% of the lungs could be inflated even at high inflation pressure (34 cmH2O), and most gas was trapped during deflation. The amount of trapped gas volume at 30 min was related to the degree of lung inflation maintained during the 5- to 30-min period after exsanguination. Since stiffness of the lung tissue was unlikely to explain the phenomenon, we speculated airway obstruction as the major factor. No foam or bubbles were found in larger airways and we thus hypothesized that the obstruction was due to bronchoconstriction. This was confirmed histologically in that the lumina of both bronchi and bronchioles were constricted. The latent period to the onset of this constriction was short (approximately 5 min). It was not associated with O2 availability but was delayed an additional 15 min by a thromboxane inhibitor (dazoxiben). Neither maintaining lung temperature at 37 degrees C nor vagotomy and/or cervical transection prevented the constriction. Without exsanguination, onset of bronchoconstriction was delayed by about 1 h. We conclude that postmortem bronchoconstriction may be caused by release of an endogenous constrictor agent.

Effects of lung inflation on alveolar epithelial solute and water transport properties

1982 ◽  
Vol 52 (6) ◽  
pp. 1498-1505 ◽  
Author(s):  
K. J. Kim ◽  
E. D. Crandall
Keyword(s):  
Transport Properties ◽  
Epithelial Transport ◽  
Rana Catesbeiana ◽  
Electrical Potential ◽  
Ringer Solution ◽  
Potential Measurement ◽  
Lung Inflation ◽  
Solute Permeability ◽  
Alveolar Epithelial

Paired hollow bullfrog lungs (Rana catesbeiana) were used to study the effects of lung inflation on alveolar epithelial transport of water and hydrophilic solutes. Frogs were double pithed and the lungs were removed after bronchial placement of a Lucite plug. Three openings in the plug accommodated the insertion of two agar-Ringer bridges (for electrical potential measurement and passage of direct current) and the injection and removal of alveolar bathing fluid. Ringer solution containing a tracer quantity of radioactive solute was instilled into the lung sacs (5 ml or 50 ml) and the lungs were suspended in baths of Ringer solution containng appropriate cold solutes (5 mM). Permeability properties of each solute (and water) were determined from the rate of radiotracer concentration change in the bath. The spontaneous potential difference, tissue resistance, and solute permeability properties determined in these experiments showed no significant differences between the 5- and 50-ml lungs. Assuming homogeneous, cylindrical water-filled pores to be present in the tissue, the equivalent pore radii estimated from the rates of solute and water fluxes were 1.1 (for 5-ml lungs) and 0.9 nm (for 50-ml lungs). After overinflation of the lung (to greater than 80 ml), experiments at 50 ml yielded a pore radius of 3.4 nm. These data suggest that passive alveolar epithelial transport properties do not change with degrees of lung inflation normally encountered in vivo but that overinflation can lead to increased leakiness of the barrier.

Alveolar liquid pressures in newborn and adult rabbit lungs

1988 ◽  
Vol 64 (4) ◽  
pp. 1629-1635 ◽  
Author(s):  
C. D. Fike ◽  
S. J. Lai-Fook ◽  
R. D. Bland
Keyword(s):  
Airway Pressure ◽  
Transpulmonary Pressure ◽  
Dry Weight ◽  
Adult Rabbit ◽  
Liquid Pressure ◽  
Lung Maturation ◽  
Lung Inflation ◽  
Lung Deflation ◽  
Isolated Lungs ◽  
Alveolar Liquid

To study the effects of lung maturation and inflation on alveolar liquid pressures, we isolated lungs from adult and newborn rabbit pups (1-11 days old). We used the micropuncture technique to measure alveolar liquid pressure at several transpulmonary pressures on lung deflation. Alveolar liquid pressure was greater than pleural pressure but less than airway pressure at all transpulmonary pressures. Alveolar liquid pressure decreased further below airway pressure with lung inflation. At high transpulmonary pressure, alveolar liquid pressure was less in newborn than in adult lungs. To study the effects of edema, we measured alveolar liquid pressures in newborn lungs with different wet-to-dry weight ratios. Alveolar liquid pressure increased with progressive edema. In addition, we compared alveolar liquid and perivenular interstitial pressures in perfused newborn lungs and found that they were similar. Thus alveolar liquid pressure can be used to estimate perivenular interstitial pressure. We conclude that the transvascular pressure gradient for fluid flux into the interstitium might increase with lung inflation and decrease with progressive edema. Furthermore, this gradient might be greater in newborn than adult lungs at high inflation pressures.

Alveolar edema dispersion and alveolar protein permeability during high volume ventilation: effect of positive end-expiratory pressure

2007 ◽  
Vol 33 (4) ◽  
pp. 711-717 ◽  
Author(s):  
Nicolas de Prost ◽  
Damien Roux ◽  
Didier Dreyfuss ◽  
Jean-Damien Ricard ◽  
Dominique Le Guludec ◽  
...  
Keyword(s):  
High Volume ◽  
Positive End Expiratory Pressure ◽  
Volume Ventilation ◽  
Protein Permeability ◽  
Alveolar Edema

Invited Review: Alveolar edema fluid clearance in the injured lung

2002 ◽  
Vol 93 (6) ◽  
pp. 2207-2213 ◽  
Author(s):  
Yves Berthiaume ◽  
Hans G. Folkesson ◽  
Michael A. Matthay
Keyword(s):  
Lung Injury ◽  
Sodium Transport ◽  
Molecular Mechanisms ◽  
Chloride Transport ◽  
Edema Fluid ◽  
Injured Lung ◽  
Transport Molecules ◽  
Alveolar Liquid Clearance ◽  
Alveolar Edema ◽  
Alveolar Liquid

Resolution of pulmonary edema involved active transepithelial sodium transport. Although several of the cellular and molecular mechanisms involved are relatively well understood, it is only recently that the regulation of these mechanisms in injured lung are being evaluated. Interestingly, in mild-to-moderate lung injury, alveolar edema fluid clearance is often preserved. This preserved or enhanced alveolar fluid clearance is mediated by catecholamine-dependent or -independent mechanisms. This stimulation of alveolar liquid clearance is related to activation or increased expression of sodium transport molecules such as the epithelial sodium channel or the Na+-K+-ATPase pump and may also involve the cystic fibrosis transmembrane conductance regulator. When severe lung injury occurs, the decrease in alveolar liquid clearance may be related to changes in alveolar permeability or to changes in activity or expression of sodium or chloride transport molecules. Multiple pharmacological tools such as β-adrenergic agonists, vasoactive drugs, or gene therapy may prove effective in stimulating the resolution of alveolar edema in the injured lung.

scholarly journals Impaired alveolar liquid clearance after 48-h isoproterenol infusion spontaneously recovers by 96 h of continuous infusion

2006 ◽  
Vol 291 (2) ◽  
pp. L252-L256 ◽  
Author(s):  
Michael B. Maron ◽  
Hans G. Folkesson ◽  
Sonya M. Stader ◽  
Cheryl M. Hodnichak
Keyword(s):  
Continuous Infusion ◽  
Time Course ◽  
Lung Epithelium ◽  
Osmotic Minipump ◽  
Peripheral Lung ◽  
Distal Lung ◽  
Time Periods ◽  
Isoproterenol Infusion ◽  
Alveolar Liquid Clearance ◽  
Alveolar Liquid

We previously demonstrated that 48-h isoproterenol (Iso) infusion in rats impaired the ability of β-adrenoceptor (β-AR) agonists to increase alveolar liquid clearance (ALC). In this study, we determined whether this impairment persisted over longer time periods by infusing 400 μg·kg−1·h−1 Iso by osmotic minipump for 24–144 h ( n = 6–7/group). ALC in control rats was 19.0 ± 2.4 (SD)% of instilled volume absorbed per hour. In Iso-infused rats, ALC was elevated at 24 h (34.9 ± 2.4%) and decreased at 48 h (15.2 ± 4.4%) and had recovered to 24 h values at 96 h (37.3 ± 3.8%) and 144 h (35.2 ± 3.3%). Plasma Iso concentrations remained elevated at all Iso infusion times. Peripheral lung β2-AR expression exhibited a parallel time course, with a reduction in expression observed at 48 h, followed by an increase to 24 h values at 96 and 144 h. Propranolol prevented the increase in ALC observed at 96 and 144 h, indicating that the recovery in ALC was mediated by a recovery of β-AR function and β-AR signaling. ALC at 96 and 144 h could not be further increased by terbutaline, indicating that ALC was maximally stimulated. These data indicate that recovery of β-AR-stimulated ALC can occur in the continued presence of Iso and is mediated by a recovery of the ability of the distal lung epithelium to respond to β-AR stimulation.

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