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.

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.

scholarly journals Procoagulant alveolar microparticles in the lungs of patients with acute respiratory distress syndrome

2009 ◽  
Vol 297 (6) ◽  
pp. L1035-L1041 ◽  
Author(s):  
Julie A. Bastarache ◽  
Richard D. Fremont ◽  
Jonathan A. Kropski ◽  
Frederick R. Bossert ◽  
Lorraine B. Ware
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Alveolar Epithelium ◽  
Procoagulant Activity ◽  
Alveolar Epithelial ◽  
Potential Source ◽  
Air Space

Coagulation and fibrinolysis abnormalities are observed in acute lung injury (ALI) in both human disease and animal models and may contribute to ongoing inflammation in the lung. Tissue factor (TF), the main initiator of the coagulation cascade, is upregulated in the lungs of patients with ALI/acute respiratory distress syndrome (ARDS) and likely contributes to fibrin deposition in the air space. The mechanisms that govern TF upregulation and activation in the lung are not well understood. In the vascular space, TF-bearing microparticles (MPs) are central to clot formation and propagation. We hypothesized that TF-bearing MPs in the lungs of patients with ARDS contribute to the procoagulant phenotype in the air space during acute injury and that the alveolar epithelium is one potential source of TF MPs. We studied pulmonary edema fluid collected from patients with ARDS compared with a control group of patients with hydrostatic pulmonary edema. Patients with ARDS have higher concentrations of MPs in the lung compared with patients with hydrostatic edema (25.5 IQR 21.3–46.9 vs. 7.8 IQR 2.3–27.5 μmol/l, P = 0.009 by Mann-Whitney U-test). These MPs are enriched for TF, have procoagulant activity, and likely originate from the alveolar epithelium [as measured by elevated levels of RAGE (receptor for advanced glycation end products) in ARDS MPs compared with hydrostatic MPs]. Furthermore, alveolar epithelial cells in culture release procoagulant TF MPs in response to a proinflammatory stimulus. These findings suggest that alveolar epithelial-derived MPs are one potential source of TF procoagulant activity in the air space in ARDS and that epithelial MP formation and release may represent a unique therapeutic target in ARDS.

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.

Equivalent pore estimate for the alveolar-airway barrier in isolated dog lung

1988 ◽  
Vol 64 (3) ◽  
pp. 1134-1142 ◽  
Author(s):  
R. L. Conhaim ◽  
A. Eaton ◽  
N. C. Staub ◽  
T. D. Heath
Keyword(s):  
High Pressure ◽  
Pulmonary Edema ◽  
Intercellular Junctions ◽  
Model Fit ◽  
Epithelial Injury ◽  
Pore Model ◽  
Liquid Flux ◽  
Air Space ◽  
Lung Lobes

In high-pressure pulmonary edema, lung interstitial and air space edema liquids have equal protein concentrations (Am. J. Physiol. 231: 1466, 1976). This suggests that the alveolar-airway barrier separating the air and interstitial spaces is relatively unrestrictive, even without apparent epithelial injury. To estimate the equivalent pore population of the alveolar-airway barrier we inflated each of 18 isolated dog lung lobes for 1 h with a solution of colored tracer of uniform radius. Tracer radii ranged from 1.3 to 405 nm. After freezing the lobes in liquid N2, we measured interstitial tracer concentrations in frozen perivascular cuffs or in samples thawed after dissection from frozen cuffs. Relative to the concentrations instilled, interstitial concentrations ranged from 0.34 for the smallest particles (1.3 and 3.5 nm radius) to zero for particles with radii of 405 nm. From the results we designed a pore model of the alveolar-airway barrier to reproduce the concentrations we measured. No single-pore model could be obtained, although a three-pore model fit the data well. The model results predict that pores with radii of 1, 40, and 400 nm would account for 68, 30, and 2% of total liquid flux, respectively. The majority of liquid flux (68%) would occur through passageways smaller than the smallest tracer we used (1.3 nm radius). We believe the alveolar-airway barrier consists not only of tight intercellular junctions that allow passage of only water and electrolytes but also of a smaller number of large leaks that allow passage of particles up to nearly 400 nm in radius.

PEEP inhibits hypoxic pulmonary vasoconstriction in dogs

1991 ◽  
Vol 70 (4) ◽  
pp. 1867-1873 ◽  
Author(s):  
P. Lejeune ◽  
J. L. Vachiery ◽  
J. M. De Smet ◽  
M. Leeman ◽  
S. Brimioulle ◽  
...  
Keyword(s):  
Inferior Vena ◽  
Intact Animal ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Balloon Catheter ◽  
Vena Cava ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial

The effects of an increase in alveolar pressure on hypoxic pulmonary vasoconstriction (HPV) have been reported variably. We therefore studied the effects of positive end-expiratory pressure (PEEP) on pulmonary hemodynamics in 13 pentobarbital-anesthetized dogs ventilated alternately in hyperoxia [inspired O2 fraction (FIO2) 0.4] and in hypoxia (FIO2 0.1). In this intact animal model, HPV was defined as the gradient between hypoxic and hyperoxic transmural (tm) mean pulmonary arterial pressure [Ppa(tm)] at any level of cardiac index (Q). Ppa(tm)/Q plots were constructed with mean transmural left atrial pressure [Pla(tm)] kept constant at approximately 6 mmHg (n = 5 dogs), and Ppa(tm)/PEEP plots were constructed with Q kept constant approximately 2.8 l.min-1.m-2 and Pla(tm) kept constant approximately 8 mmHg (n = 8 dogs). Q was manipulated using a femoral arteriovenous bypass and a balloon catheter in the inferior vena cava. Pla(tm) was held constant by a balloon catheter placed by left thoracotomy in the left atrium. Increasing PEEP, from 0 to 12 Torr by 2-Torr increments, at constant Q and Pla(tm), increased Ppa(tm) from 14 +/- 1 (SE) to 19 +/- 1 mmHg in hyperoxia but did not affect Ppa(tm) (from 22 +/- 2 to 23 +/- 1 mmHg) in hypoxia. Both hypoxia and PEEP, at constant Pla(tm), increased Ppa(tm) over the whole range of Q studied, from 1 to 5 l/min, but more at the highest than at the lowest Q and without change in extrapolated pressure intercepts. Adding PEEP to hypoxia did not affect Ppa(tm) at all levels of Q.(ABSTRACT TRUNCATED AT 250 WORDS)

"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.

Cardiovascular Responses to Pressure Alterations Within the Urinary Tract of the Dog

1958 ◽  
Vol 193 (2) ◽  
pp. 260-262 ◽  
Author(s):  
Leonard B. Berman ◽  
John C. Rose
Keyword(s):  
Urinary Tract ◽  
Right Ventricular ◽  
Normal Saline ◽  
Cardiovascular Responses ◽  
Marked Contrast ◽  
Anesthetized Dogs ◽  
Acute Changes

Acute changes in pressure within the bladders and renal pelves of intact, anesthetized dogs were produced by the infusion of normal saline. Direct and continuous observations were made of aortic, right ventricular and intravesical or intrapelvic pressures, as well as the electrocardiogram. No significant cardiovascular alterations were observed during acute and extreme increments and decrements of intraluminal urinary tract pressures. These results are in marked contrast with those seen in reptilia and amphibia.

Mechanisms and regulation of ion transport in adult mammalian alveolar type II pneumocytes

1991 ◽  
Vol 261 (5) ◽  
pp. C727-C738 ◽  
Author(s):  
S. Matalon
Keyword(s):  
Epithelial Transport ◽  
Cultured Cells ◽  
Basolateral Membrane ◽  
Alveolar Epithelium ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Epithelial Lining ◽  
Epithelial Lining Fluid

The adult alveolar epithelium consists of type I and type II (ATII) pneumocytes that form a tight barrier, which severely restricts the entry of lipid-insoluble molecules from the interstitial to the alveolar space. Current in vivo and in vitro evidence indicates that the alveolar epithelium is also an absorptive epithelium, capable of transporting Na+ from the alveolar lumen, which is bathed by a small amount of epithelial lining fluid, to the interstitial space. The in situ localization of Na(+)-K(+)-ATPase activity in ATII cells and the fact that these cells are involved in a number of crucial functions, such as surfactant secretion and alveolar remodeling after injury, led investigators to examine their transport characteristics. Radioactive flux studies, in both freshly isolated and cultured cells, and bioelectric measurements in ATII cells grown on porous supports indicate that they transport Na+ according to the Koefoed-Johnsen and Ussing model of epithelial transport. Na+ enters the apical membrane, because of the favorable electrochemical gradient, through Na+ cotransporters, a Na(+)-H+ antiport, and cation channels and is pumped across the basolateral membrane by a ouabain-sensitive Na(+)-K+ pump. Na+ transport is enhanced by substances that increase intracellular adenosine 3',5'-cyclic monophosphate. In addition to Na+ transporters, ATII cells contain several transporters that regulate their intracellular pH, including a H(+)-ATPase, which may explain the low pH of the epithelial lining fluid. The absorptive properties of ATII cells may play an important role in regulating the degree of alveolar fluid in health and disease.

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