Effect of lung inflation on alveolar-airway barrier protein permeability in dog lung

To determine the leakiness to protein of the barrier that separates the air space and interstitial compartment of the lung, we measured perivascular interstitial fluid cuff protein concentration and volume in 10 isolated and 9 intact closed-chest dog lung lobes, which we degassed and inflated to 25, 50, 75, or 100% of capacity with 5% bovine serum albumin labeled with Evans blue dye. After 1 h we froze the lobes in liquid N2 and made color transparencies of 20 randomly selected frozen samples of each lobe. We measured Evans blue dye-albumin concentrations from absorption by cuff images of a 50-micron-diam red (lambda = 620 nm) microspot. We measured absolute cuff volume (ml/g dry lung) by point counting on the transparencies. Using specific Evans blue-albumin fluorescence we determined that the dye was protein bound in airways and cuffs. Cuff protein concentration averaged 37% of instillate concentration and did not vary with inflation volume or between isolated and intact lobes. Cuff volume was 3.4 ml/g dry lung at total lung capacity in both isolated and intact lobes. We conclude that at some point the barrier is permeable to albumin as well as liquid at all lung volumes in dogs and that the protein sieving properties of the barrier do not change with lung expansion over the range examined. The liquid storage capacity of the cuffs can increase as much as 20-fold between low and high lung volumes.

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Exogenous Surfactant Preserves Lung Function and Reduces Alveolar Evans Blue Dye Influx in a Rat Model of Ventilation-induced Lung Injury

Anesthesiology ◽

10.1097/00000542-199808000-00024 ◽

1998 ◽

Vol 89 (2) ◽

pp. 467-474 ◽

Cited By ~ 34

Author(s):

Serge J. C. Verbrugge ◽

Gilberto Vazguez de Anda ◽

Diederik Gommers ◽

Sabastian J. C. M. M. Neggers ◽

Vera MSc Sorm ◽

...

Keyword(s):

Surface Tension ◽

Bronchoalveolar Lavage ◽

Minimal Surface ◽

Evans Blue ◽

High Peak ◽

Exogenous Surfactant ◽

Blue Dye ◽

Lung Volumes ◽

Intratracheal Administration ◽

Evans Blue Dye

Background Changes in pulmonary edema infiltration and surfactant after intermittent positive pressure ventilation with high peak inspiratory lung volumes have been well described. To further elucidate the role of surfactant changes, the authors tested the effect of different doses of exogenous surfactant preceding high peak inspiratory lung volumes on lung function and lung permeability. Methods Five groups of Sprague-Dawley rats (n = 6 per group) were subjected to 20 min of high peak inspiratory lung volumes. Before high peak inspiratory lung volumes, four of these groups received intratracheal administration of saline or 50, 100, or 200 mg/kg body weight surfactant; one group received no intratracheal administration. Gas exchange was measured during mechanical ventilation. A sixth group served as nontreated, nonventilated controls. After death, all lungs were excised, and static pressure-volume curves and total lung volume at a transpulmonary pressure of 5 cm H2O were recorded. The Gruenwald index and the steepest part of the compliance curve (Cmax) were calculated. A bronchoalveolar lavage was performed; surfactant small and large aggregate total phosphorus and minimal surface tension were measured. In a second experiment in five groups of rats (n = 6 per group), lung permeability for Evans blue dye was measured. Before 20 min of high peak inspiratory lung volumes, three groups received intratracheal administration of 100, 200, or 400 mg/ kg body weight surfactant; one group received no intratracheal administration. A fifth group served as nontreated, nonventilated controls. Results Exogenous surfactant at a dose of 200 mg/kg preserved total lung volume at a pressure of 5 cm H2O, maximum compliance, the Gruenwald Index, and oxygenation after 20 min of mechanical ventilation. The most active surfactant was recovered in the group that received 200 mg/kg surfactant, and this dose reduced minimal surface tension of bronchoalveolar lavage to control values. Alveolar influx of Evans blue dye was reduced in the groups that received 200 and 400 mg/kg exogenous surfactant. Conclusions Exogenous surfactant preceding high peak inspiratory lung volumes prevents impairment of oxygenation, lung mechanics, and minimal surface tension of bronchoalveolar lavage fluid and reduces alveolar influx of Evans blue dye. These data indicate that surfactant has a beneficial effect on ventilation-induced lung injury.

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Evans Blue Dye as an in vivo marker of myofibre damage: optimising parameters for detecting initial myofibre membrane permeability

Journal of Anatomy ◽

10.1046/j.0021-8782.2001.00008.x ◽

2002 ◽

Vol 200 (1) ◽

pp. 69-79 ◽

Cited By ~ 190

Author(s):

P. W. Hamer ◽

J. M. McGeachie ◽

M. J. Davies ◽

M. D. Grounds

Keyword(s):

Membrane Permeability ◽

Evans Blue ◽

Blue Dye ◽

Evans Blue Dye

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Regional Deposition of Inhaled Evans Blue Dye in Mechanically Ventilated Rabbits with Air or Helium Oxygen Mixture

Experimental Lung Research ◽

10.3109/01902149809099580 ◽

1998 ◽

Vol 24 (2) ◽

pp. 159-172 ◽

Cited By ~ 4

Author(s):

Magnus Svartengren ◽

Patrik Skogward ◽

Ola Nerbrink ◽

Magnus Dahlbäck

Keyword(s):

Evans Blue ◽

Oxygen Mixture ◽

Blue Dye ◽

Mechanically Ventilated ◽

Evans Blue Dye ◽

Regional Deposition

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Acoustic enhanced Evans blue dye perfusion in neurological tissues

10.1121/1.2890703 ◽

2007 ◽

Cited By ~ 1

Author(s):

George K. Lewis Jr. ◽

Willam L. Olbricht ◽

George Lewis

Keyword(s):

Evans Blue ◽

Blue Dye ◽

Evans Blue Dye

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Flow of edema fluid into pulmonary airways

Journal of Applied Physiology ◽

10.1152/jappl.1983.55.4.1262 ◽

1983 ◽

Vol 55 (4) ◽

pp. 1262-1268 ◽

Cited By ~ 5

Author(s):

G. R. Mason ◽

R. M. Effros

Keyword(s):

Evans Blue ◽

Left Atrial ◽

Blue Dye ◽

Edema Formation ◽

Evans Blue Dye ◽

Colloid Particles ◽

Edema Fluid ◽

Pulmonary Airways ◽

99Mtc Sulfur Colloid

An in situ rabbit preparation was used to characterize the manner in which edema fluid enters the airways when left atrial pressures are elevated. The airways were initially filled with fluid to minimize retrograde flow of edema fluid into the alveoli. The airway solution contained 125I-albumin and in some studies [14C]sucrose, and the lungs were perfused with a comparable solution which contained albumin labeled with Evans blue dye and 99mTc-diethylenetriaminepentaacetate (DTPA) or 99mTc-sulfur-colloid particles (0.4-1.7 micron diam). After 30 min of perfusion, fluid was pumped from the airways into serial tubes. When left atrial pressures were low, there was very little transfer of labels detectable between the airway and perfusate solutions. However when left atrial pressures were increased to either 15 or 22 cmH2O, fluid entered the airways containing approximately the same concentrations of Evans blue dye and 99mTc-DTPA as those present in the perfusate. In contrast, the concentration of colloid particles averaged less than 5% perfusate concentrations, indicating that the fluid had not escaped through a tear in the barriers separating the vascular and airway compartments. Concentrations of the perfusate fluid and indicators were highest in the initial samples pumped from the airways. These observations suggest that some of the fluid entering the airways may be derived from peribronchial cuffs or that there are marked regional differences in edema formation from alveoli.

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A modified bioassay for heat-stable Escherichia coli enterotoxin

Canadian Journal of Microbiology ◽

10.1139/m77-049 ◽

1977 ◽

Vol 23 (3) ◽

pp. 331-336 ◽

Cited By ~ 8

Author(s):

S. Stavric ◽

D. Jeffrey

Keyword(s):

Escherichia Coli ◽

Body Weight ◽

Incubation Time ◽

Evans Blue ◽

Room Temperature ◽

Blue Dye ◽

Evans Blue Dye ◽

Heat Stable ◽

Stomach Distention ◽

Time Required

Infant mice were injected orally with preparations containing Escherichia coli heat-stable enterotoxin (ST) and Evans blue dye, and incubated at 22 °C. With enterotoxin-positive samples, the stomach was distended and contained essentially all of the dye. With enterotoxin-negative samples, the stomach remained normal in size and the dye passed freely into the intestines. The time required to obtain the maximum ratio of gut weight to body weight varied from 30 to 90 min and was dependent upon the concentration of enterotoxin. Heat-labile enterotoxin (LT) had no effect during this period.Based on these findings, the mouse incubation time was reduced from 4 h to 90 min, and the heating of test samples was retained only for confirmation of ST. The location of the dye and stomach distention served as an indicator of positive responses to ST. Incubation of the mice at room temperature (22 °C) was found satisfactory.

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A Study of the Pathogenesis and Prevention of Central Pontine Myelinolysis in a Rat Model

Journal of International Medical Research ◽

10.1177/147323000603400305 ◽

2006 ◽

Vol 34 (3) ◽

pp. 264-271 ◽

Cited By ~ 6

Author(s):

Q-H Ke ◽

T-B Liang ◽

J Yu ◽

S-S Zheng

Keyword(s):

Hypertonic Saline ◽

Blood Brain Barrier ◽

Evans Blue ◽

Central Pontine Myelinolysis ◽

Brain Barrier ◽

Blue Dye ◽

Evans Blue Dye ◽

Pontine Myelinolysis ◽

Demyelinating Lesions ◽

Central Pontine

The development of central pontine myelinolysis was studied in rats. Severe hyponatraemia was induced using vasopressin tannate and 2.5% dextrose in water and then rapidly corrected with hypertonic saline alone, hypertonic saline and dexamethasone simultaneously, or hypertonic saline plus dexamethasone 24 h later. The permeability of the blood-brain barrier was evaluated using the extravasation of Evans blue dye and the expression of inducible nitric oxide synthase (iNOS) in the brain was examined using Western blot analysis. Histological sections were examined for demyelinating lesions. In rats receiving hypertonic saline alone, Evans blue dye content and expression of iNOS began to increase 6 and 3 h, respectively, after rapid correction of hyponatraemia and demyelinating lesions were seen. When dexamethasone was given simultaneously with hypertonic saline, these increases were inhibited and demyelinating lesions were absent. These effects were lost if dexamethasone injection was delayed. Disruption of the blood-brain barrier and increased iNOS expression may be involved in the pathogenesis of central pontine myelinolysis, and early treatment with dexamethasone may help prevent the development of central pontine myelinolysis.

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