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.

Solute permeability of the alveolar epithelium in alloxan edema in dogs

1978 ◽  
Vol 44 (3) ◽  
pp. 353-357 ◽  
Author(s):  
R. M. Nelson ◽  
B. R. McIntyre ◽  
E. A. Egan
Keyword(s):  
Pulmonary Edema ◽  
Direct Effect ◽  
Normal Saline ◽  
Balloon Catheter ◽  
Alveolar Epithelium ◽  
Permeability Change ◽  
Epithelial Lining ◽  
Solute Permeability ◽  
Air Space ◽  
Anesthetized Dogs

The permeability of the alveolar epithelium following alloxan challenge was studied in dogs by determining transfer of radiolabeled solutes between alveolus and blood. Two days after injection of 131-Ialbumin into the blood, anesthetized dogs had the air space of part of one lung isolated by a balloon catheter lodged in a bronchus. We infused the atelectatis-isolated area with normal saline containing trace amounts of Blue Dextran, 125Ialbumin, and 57Co-cyanocobalamin; challenged six animals with intravenous alloxan, and six animals with alloxan added to the alveolar saline. During the pulmonary edema, 57Co-cyanocabalamin and 125I-albumin appeared in the blood and 131I-albumin entered the alveolar saline. The animals challenged by alveolar instillation showed a greater permeability change (P less than 0.05). The bidirectional transfer of macromolecules indicates that alloxan produces a change in the permeability of the alveolar epithelium, allowing diffusional exchange of macromolecules. Since alveolar flooding in hemodynamic edema does not show a similar change in the permeability of the epithelial lining, alveolar flooding in alloxan edema is not due solely to an effect on the endothelial membrane, but also to a direct effect on the epithelial membrane.

scholarly journals Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury

2006 ◽  
Vol 291 (3) ◽  
pp. L354-L361 ◽  
Author(s):  
Michael T. Ganter ◽  
Lorraine B. Ware ◽  
Marybeth Howard ◽  
Jérémie Roux ◽  
Brandi Gartland ◽  
...  
Keyword(s):  
Heat Shock ◽  
Pulmonary Edema ◽  
Stress Protein ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial ◽  
Edema Fluid ◽  
Protein Response ◽  
Alveolar Edema

Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The second objective was to determine whether activation of the stress protein response (SPR) caused the release of Hsp72 into the extracellular space in vivo and in vitro and to determine whether SPR activation and/or eHsp72 itself would prevent the IL-1β-mediated inhibition of the vectorial fluid transport across alveolar type II cells. We found that eHsp72 was present in plasma and pulmonary edema fluid of ALI patients and that eHsp72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, SPR activation in vivo in mice and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of Hsp72. Finally, SPR activation, but not eHsp72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1β. Thus SPR may protect the alveolar epithelium against oxidative stress associated with experimental ALI, and eHsp72 may serve as a marker of SPR activation in the distal air spaces of patients with ALI.

scholarly journals Effect of adrenalectomy on pulmonary edema resolution

2019 ◽  
Vol 42 (2) ◽  
pp. E33-37
Author(s):  
Chantal Massé ◽  
Yves Berthiaume
Keyword(s):  
Pulmonary Edema ◽  
Alveolar Epithelium ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Endogenous Catecholamines ◽  
Sodium Dependent ◽  
Corticosterone Response ◽  
Permeability Pulmonary Edema ◽  
Dependent Mechanism ◽  
Alveolar Edema

Purpose: The capacity of the lung to clear edema fluid has been shown to be one of the factors that can influence the prognosis of cardiogenic and noncardiogenic pulmonary edema. Active Na+ transport across the alveolar epithelium is the main driving force involved in this physiological process. Since endogenous catecholamines are known to activate the sodium-dependent mechanism of alveolar edema clearance, the objective of the present study was to explore if adrenalectomy, which prevents the release of endogenous catecholamines and other hormones, such as corticosterone, into circulation, would affect edema resolution in a model of lung injury induced by thiourea. Methods: A high-permeability pulmonary edema was induced in adult male Sprague-Dawley rats using a thiourea-induced pulmonary edema model. To determine if the release of adrenalin and corticosterone is essential for resolution of the thiourea-induced edema, we measured 1) the release of adrenalin and corticosterone in urine and 2) edema resolution in control animals and adrenalectomized animals. Results: The administration of thiourea significantly increased the wet-to-dry ratio after four and eight hours. After 12 and 24 hours, the wet-to-dry ratio gradually returned to baseline. Although thiourea-induced pulmonary edema was associated with a significant increase in urine adrenalin and corticosterone, the absence of adrenalin and corticosterone response in adrenalectomized animals did not prevent the resolution of the edema. Conclusions: These experiments demonstrated that resolution of thioureainduced pulmonary edema can occur in the absence of hormonal secretion by the adrenal glands.

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.

Effects of 100% O2 breathing on permeability of alveolar epithelium to solute

1981 ◽  
Vol 50 (4) ◽  
pp. 859-863 ◽  
Author(s):  
S. Matalon ◽  
E. A. Egan
Keyword(s):  
Cytochrome C ◽  
Pulmonary Edema ◽  
Lower Lobe ◽  
Alveolar Epithelium ◽  
Alveolar Space ◽  
Lung Weight ◽  
Air Breathing ◽  
Solute Permeability ◽  
Arterial Blood ◽  
The Right

We measured the effects of 100% O2 exposure at 1 atm for 48 (n = 5) and 63 h (n = 6) on the solute permeability of the alveolar epithelium of rabbits. We instilled 10-15 ml of saline containing trace amounts of 131I-albumin (r approximately 35 A), 125I-cytochrome c (r approximately 17 A), and [57Co]cyanocobalamin (r approximately 6.5 A) into an atelectatic segment of the right lower lobe. Egress of these tracers was determined from their change in concentration in the alveolar saline and their detection in arterial blood. All tracers left the alveolar space and appeared in the arterial blood on the 63-h O2 group, cytochrome c and cyanocobalamin in the 48-h O2 group, and only cyanocobalamin in the control (air breathing). The O2-exposed animals had PaO2 values higher than 500 Torr, normal PaCO2 and pH, and wet-to-dry lung weight ratios not different from control. We concluded that increasing the length of O2 exposure increases the solute permeability of the alveolar epithelium and this precedes the appearance of pulmonary edema.

"Closing volume" changes in alloxan-induced pulmonary edema in anesthetized dogs

1975 ◽  
Vol 39 (2) ◽  
pp. 235-241 ◽  
Author(s):  
R. Lemen ◽  
J. G. Jones ◽  
P. D. Graf ◽  
G. Cowan
Keyword(s):  
Pulmonary Edema ◽  
Control Group ◽  
Closing Volume ◽  
Base Line ◽  
Alveolar Plateau ◽  
Single Breath ◽  
Period 2 ◽  
System Pressure ◽  
Before And After ◽  
Anesthetized Dogs

“Closing volume” (CV) was measured by the single-breath oxygen (SBO2) test in six dogs (alloxan group) before and after alloxan 100–200 mg/kg iv) was injected. CV increased significantly (P less than 0.05) from 32 +/- 3.2% (base line) to 45 +/- 3.5 % in period 1 (0–30 min after alloxan), but vital capacity (VC), respiratory system pressure volume (PV) curves, and alveolar plateau slopes did not change. No radiologic evidence of pulmonary edema was demonstrated in two dogs studied in period 1. CV decreased to 20 +/- 3.9% during period 2 (30–80 min after alloxan) and was associated with tracheal frothing, decreased VC, changes in the PV curve, and alveolar plateau slope, as well as histologic evidence of severe pulmonary edema. CV was 29 +/- 3.0%, and there were no changes in VC, PV curves, or alveolar plateau slopes in 6 other dogs studied for 2 h (control group). CV increased during period 1 before pulmonary edema could be demonstrated by changes in VC, PV curves, or radiography, but in period 2 lung function was so altered that CV by the SBO2 technique gave no useful information.

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.

Hydraulic conductivity of canine parietal pleura in vivo

1990 ◽  
Vol 69 (2) ◽  
pp. 438-442 ◽  
Author(s):  
D. Negrini ◽  
M. I. Townsley ◽  
A. E. Taylor
Keyword(s):  
Hydraulic Conductivity ◽  
Chest Wall ◽  
Body Position ◽  
Linear Regression Analysis ◽  
Isotonic Saline ◽  
Parietal Pleura ◽  
Autologous Plasma ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

The hydraulic conductivity (Lp) of the parietal pleura was measured in vivo in spontaneously breathing anesthetized dogs in either the supine (n = 8) or the prone (n = 7) position and in an excised portion of the chest wall in which the pleura and its adjacent tissue were intact (n = 3). A capsule was glued to the exposed parietal pleura after the intercostal muscles were removed. The capsule was filled with either autologous plasma or isotonic saline. Transpleural fluid flow (V) was measured at several transpleural hydrostatic pressures (delta P) from the rate of meniscus movement within a graduated pipette connected to the capsule. Delta P was defined as the measured difference between capsule and pleural liquid pressures. The Lp of the parietal pleura was calculated from the slope of the line relating V to delta P by use of linear regression analysis. Lp in vivo averaged 1.36 X 10(-3) +/- 0.45 X 10(-3) (SD) ml.h-1.cmH2O-1.cm-2, regardless of whether the capsule was filled with plasma or saline and irrespective of body position. This value was not significantly different from that measured in the excised chest wall preparation (1.43 X 10(-3) +/- 1.1 X 10(-3) ml.h-1.cmH2O-1.cm-2). The parietal pleura offers little resistance to transpleural protein movement, because there was no observed difference between plasma and saline. We conclude that because the Lp for intact parietal pleura and extrapleural interstitium is approximately 100 times smaller than that previously measured in isolated stripped pleural preparations, removal of parietal pleural results in a damaged preparation.

Effect of regional inhomogeneity on collateral airway resistance

1984 ◽  
Vol 57 (1) ◽  
pp. 254-261 ◽  
Author(s):  
S. D. Fuller ◽  
N. E. Robinson
Keyword(s):  
Airway Resistance ◽  
Transpulmonary Pressure ◽  
Double Lumen ◽  
Double Lumen Catheter ◽  
Lung Segment ◽  
Peripheral Airway ◽  
Lumen Catheter ◽  
Anesthetized Dogs ◽  
Relationship Of ◽  
Regional Inhomogeneity

We studied the interaction of transpulmonary pressure (Pao) and the pressure in an isolated sublobar lung segment (Ps) on collateral resistance (Rcoll) in excised dog lungs. A double-lumen catheter was advanced through the trachea and wedged in a peripheral airway. Gas flowed through the outer lumenof the catheter (Vcoll) to enter the segment while Ps was measured by the inner lumen. Collateral resistance was calculated as Rcoll = (Ps - Pao)/Vcoll. At constant Ps, raising Pao sharply decreased Rcoll, but at constant Pao, raising Ps increased Rcoll. Replotting these data showed that Rcoll was related to the pressure difference between the segment and the remainder of the lobe (Ps - Pao), such that raising Ps - Pao caused no change in Rcoll at lower Pao but increased Rcoll at higher Pao. Similarfindings occurred in the lungs of closed-chest anesthetized dogs. We propose that this technique measures the sum of resistances of airways and collateral channels found in the segment body (Rs) and of those passing through the segment-lobar parenchymal interface (Ri). Raising Ps - Pao decreases Rs because of the volume dependency of airway resistance and increases Ri due to tissue distortion at the interface occurring as a result of inhomogeneous segment inflation. The net change in measured Rcoll depends on which of its components change in greatest magnitude. This effect varies with Pao due to thehyperbolic relationship of Pao with airway and collateral resistance.

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