Airway level at which edema liquid enters the air space of isolated dog lungs

1989 ◽  
Vol 67 (6) ◽  
pp. 2234-2242 ◽  
Author(s):  
R. L. Conhaim
Keyword(s):  
High Pressure ◽  
Pulmonary Edema ◽  
Alternative Explanation ◽  
Albumin Solution ◽  
Liquid Flux ◽  
Air Space ◽  
Lung Periphery ◽  
Additional Lobes ◽  
Horizontal Layers ◽  
Lung Lobes

To identify lung units associated with liquid leakage into the air space in high-pressure pulmonary edema, we perfused air-inflated dog lung lobes with albumin solution to fill the loose peribronchovascular interstitium. Next, we perfused the lobes for 90 s with fluorescent albumin solution then froze the lobes in liquid nitrogen. This procedure confined the fluorescent perfusate to the liquid flux pathway between the circulation and the air space and eliminated the previously filled peribronchovascular cuffs as a source of the fluorescence that entered the air space. We divided each frozen lobe into three horizontal layers and prepared fluorescence-microscopic sections of each layer. In the most apical layers where alveolar flooding was minimal, 10.6 +/- 21.0% (SD) of alveolar ducts were either fluorescence filled or air filled and continuous with fluorescence-filled alveoli. In the same layers, 11.0 +/- 19.0% of respiratory bronchioles were similarly labeled. No terminal bronchioles in these layers were fluorescence labeled. This suggested that the fluorescent albumin entered the air space across the epithelium of respiratory bronchioles, alveolar ducts, or their associated alveoli. To simulate an alternative explanation, i.e., that fluorescence first entered central airways then flowed into peripheral air spaces, we prepared two additional lobes that we first partially inflated with fluorescent albumin then filled to capacity with air. This pushed the fluorescent solution along the airways into the lung periphery. In these lobes the ciliary lining of bronchi and terminal bronchioles was fluorescence coated. By comparison, cilia in fluorescence-perfused lobes were not coated. We conclude that alveolar flooding in hydrostatic pulmonary edema occurs across the epithelium of alveolar ducts, respiratory bronchioles, or their associated alveoli.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

Perfusion of lung periphery: effects of local exposures to ozone and pressure

1986 ◽  
Vol 61 (2) ◽  
pp. 640-646
Author(s):  
A. N. Freed ◽  
U. A. Scheffel ◽  
L. J. Kelly ◽  
B. Bromberger-Barnea ◽  
H. A. Menkes
Keyword(s):  
High Pressure ◽  
Pulmonary Perfusion ◽  
Alveolar Pressure ◽  
Anesthetized Dogs ◽  
Lung Periphery ◽  
Airways Reactivity ◽  
Collateral System

Following ozone (O3) exposure, airways reactivity increases. We investigated the possibility that exposure to O3 causes a decrease in pulmonary perfusion, and that this decrease is associated with the increase in reactivity. Perfusion was measured with radiolabeled microspheres. A wedged bronchoscope was used to isolate sublobar segments in the middle and lower lobes of anesthetized dogs. Isolated segments were exposed to either O3 or an elevated alveolar pressure. Although increased alveolar pressure decreased microsphere density, exposure to 1 ppm O3 did not. Collateral system resistance rose significantly following exposure to O3 and to high pressure. These studies do not support the hypothesis that pulmonary perfusion is decreased following O3 exposure and is associated with subsequent increases in reactivity.

Pulmonary Reflexes in Pulmonary Edema?

1957 ◽  
Vol 189 (1) ◽  
pp. 132-136 ◽  
Author(s):  
C. Aravanis ◽  
A. Libretti ◽  
E. Jona ◽  
J. F. Polli ◽  
C. K. Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
High Pressure ◽  
Nervous System ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Veins ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Additional Element ◽  
Stimulation Of

The mechanism of pulmonary edema caused by stimulation of the central nervous system was studied in 33 dogs. Stimulation was obtained by the intracisternal injection of veratrine, or of air or saline under high pressure, or by electric stimulation of the hypothalamus. Pressure changes in the pulmonary artery, left atrium and left ventricle were recorded by means of three catheters introduced through the right external jugular vein and the left femoral artery. Experiments were performed with closed or open chest, and following ligation of the thoracic aorta and inferior cava. Lung opacity was studied as a means to estimate the blood content of this organ. Data obtained in closed-chest experiments suggest that a blood shift from the systemic to the pulmonary circulation may be a factor in veratrine-induced pulmonary edema. This was confirmed by the observation that, following mechanical exclusion of the systemic circulation, no pulmonary edema occurred while the changes of left ventricular pressure were minimal and inconstant. In these animals, pulmonary artery pressure still rose indicating vasoconstriction while an increase of lung opacity suggested that the vasoconstriction was greater in the pulmonary veins than in the arteries. Injection of air or saline under high pressure into the cisterna magna and faradic stimulation of the hypothalamus caused pulmonary hypertension, even after exclusion of the systemic circulation. In these experiments, a decreased lung opacity suggested that the pulmonary constriction was greater on the arterial than on the venous side. These findings are offered as evidence that the caliber of the pulmonary vessels may be influenced by central nervous system stimulation, an additional element to be considered in the mechanism of pulmonary edema.

Interaction of chemical and high vascular pressure injury in isolated canine lung

1990 ◽  
Vol 69 (5) ◽  
pp. 1657-1664 ◽  
Author(s):  
M. I. Townsley ◽  
E. H. Lim ◽  
T. M. Sahawneh ◽  
W. Song
Keyword(s):  
High Pressure ◽  
Oleic Acid ◽  
Reflection Coefficient ◽  
Venous Pressure ◽  
Recovery Period ◽  
Total Proteins ◽  
Pressure Threshold ◽  
Capillary Filtration Coefficient ◽  
Pressure Injury ◽  
Lung Lobes

Because both chemical and mechanical insults to the lung may occur concomitantly with trauma, we hypothesized that the pressure threshold for vascular pressure-induced (mechanical) injury would be decreased after a chemical insult to the lung. Normal isolated canine lung lobes (N, n = 14) and those injured with either airway acid instillation (AAI, n = 18) or intravascular oleic acid (OA, n = 25) were exposed to short (5-min) periods of elevated venous pressure (HiPv) ranging from 19 to 130 cmH2O. Before the HiPv stress, the capillary filtration coefficient (Kf,c) was 0.12 +/- 0.01, 0.27 +/- 0.03, and 0.31 +/- 0.02 ml.min-1.cmH2O-1 x 100 g-1 and the isogravimetric capillary pressure (Pc,i) was 9.2 +/- 0.3, 6.8 +/- 0.5, and 6.5 +/- 0.3 cmH2O in N, AAI, and OA lungs, respectively. However, the pattern of response to HiPv was similar in all groups: Kf,c was no different from the pre-HiPv value when the peak venous pressure (Pv) remained less than 55 cmH2O, but it increased reversibly when peak Pv exceeded 55 cmH2O (P less than 0.05). The reflection coefficient (sigma) for total proteins measured after pressure exposure averaged 0.60 +/- 0.03, 0.32 +/- 0.04, and 0.37 +/- 0.09 for N, AAI, and OA lobes respectively. However, in contrast to the result expected if pore stretching had occurred at high pressure, in all groups the sigma measured during the HiPv stress when Pv exceeded 55 cmH2O was significantly larger than that measured during the recovery period.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth rate of perivascular cuffs in liquid-inflated dog lung lobes

1986 ◽  
Vol 61 (2) ◽  
pp. 647-653 ◽  
Author(s):  
R. L. Conhaim
Keyword(s):  
Cross Sections ◽  
Time Course ◽  
Inflation Pressure ◽  
Cuff Volume ◽  
Edema Formation ◽  
Lung Capacity ◽  
A Value ◽  
Liquid Storage ◽  
Additional Lobes ◽  
Lung Lobes

In the early stages of pulmonary edema, excess liquid leaving the pulmonary exchange vessels accumulates in the peribronchovascular interstitium where it forms large peribronchovascular cuffs. The peribronchovascular interstitium therefore acts as a reservoir to protect the air spaces from alveolar flooding. The rate of liquid accumulation and the liquid storage capacity of the cuffs determine how quickly alveolar flooding is likely to follow once edema formation has begun. To measure the rate and capacity of interstitial filling we inflated 11 isolated degassed dog lung lobes with liquid to an inflation pressure of 14 cmH2O (total lung capacity) for 1–300 min, then froze the lobes in liquid N2. We made photographs of 20 randomly selected 12 X 8-mm cross sections from each lobe and measured cuff volume from the photographs by point-counting. We found that cuff volume increased from 2.2% of air-space volume after 1 min of inflation to 9.3% after 300 min. To measure the driving pressure responsible for cuff formation we used micropipettes to measure subpleural interstitial liquid pressure at the hilum of three additional lobes. With liquid inflation pressure set to 14 cmH2O interstitial pressure rose exponentially to 11.5 cmH2O. Interstitial compliance calculated from our volume and pressure measurements equaled 0.09 ml X cmH2O–1 X g wet wt-1, a value similar to that measured in air-inflated lungs. Goldberg [Am. J. Physiol. 239 (Heart Circ. Physiol. 8): H189-H198, 1980] has likened interstitial filling to the charging of a capacitor, a process that follows a monoexponential time course.(ABSTRACT TRUNCATED AT 250 WORDS)

Accurate reference measurement for postmortem lung water

1984 ◽  
Vol 56 (1) ◽  
pp. 248-253 ◽  
Author(s):  
M. Julien ◽  
M. R. Flick ◽  
J. M. Hoeffel ◽  
J. F. Murray
Keyword(s):  
High Pressure ◽  
Pulmonary Edema ◽  
Extravascular Lung Water ◽  
Blood Cells ◽  
Dry Mass ◽  
Hydroxyproline Content ◽  
Lung Water ◽  
Lung Weight ◽  
Residual Blood ◽  
Normal Lungs

To test the hypothesis that dry blood-free lung weight is increased during pulmonary edema, thereby leading to an underestimation of the ratio of extravascular lung water-to-dry lung weight, we measured postmortem lung water, dry mass, and hydroxyproline content in 33 sheep with normal lungs (n = 10), high-pressure edema (n = 9), or increased permeability edema (n = 14). Residual blood in the lung, measured using hemoglobin as the intravascular marker in all sheep, and also using 51Cr-tagged red blood cells in 24 sheep, was not different between the two methods or among the three groups of sheep. Extravascular lung water increased 64% in sheep with high-pressure edema and 82% in those with increased permeability edema compared with control values. Dry blood-free lung weight was significantly greater (33% more than control values) in sheep with increased permeability edema, causing the ratio of extravascular lung water-to-dry blood-free lung weight to underestimate accumulated lung water by about 50%. Because hydroxyproline content of the lung was not affected by edema, the ratio of extravascular lung water-to-lung hydroxyproline content was more accurate than the ratio of extravascular lung water-to-dry blood-free lung weight in the quantification of pulmonary edema.

scholarly journals Ketamine Inhibits Lung Fluid Clearance through Reducing Alveolar Sodium Transport

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Yong Cui ◽  
Hongguang Nie ◽  
Hong Ma ◽  
Lei Chen ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Clinical Evidence ◽  
Ex Vivo ◽  
A549 Cells ◽  
Intratracheal Instillation ◽  
Lung Fluid ◽  
Whole Cell Patch Clamp ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Lung Lobes

Ketamine is a broadly used anaesthetic for analgosedation. Accumulating clinical evidence shows that ketamine causes pulmonary edema with unknown mechanisms. We measured the effects of ketamine on alveolar fluid clearance in human lung lobesex vivo. Our results showed that intratracheal instillation of ketamine markedly decreased the reabsorption of 5% bovine serum albumin instillate. In the presence of amiloride (a specific ENaC blocker), fluid resolution was not further decreased, suggesting that ketamine could decrease amiloride-sensitive fraction of AFC associated with ENaC. Moreover, we measured the regulation of amiloride-sensitive currents by ketamine in A549 cells using whole-cell patch clamp mode. Our results suggested that ketamine decreased amiloride-sensitive Na+currents (ENaC activity) in a dose-dependent fashion. These data demonstrate that reduction in lung ENaC activity and lung fluid clearance following administration of ketamine may be the crucial step of the pathogenesis of resultant pulmonary edema.

Disruption of Diffusion

2017 ◽  
Author(s):  
Nayema Khan ◽  
John Pawlowski
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
Pulmonary Complications ◽  
Alveolar Space ◽  
Disease States ◽  
Pulmonary Capillary ◽  
Air Space ◽  
And Diffusion ◽  
Pulmonary Status ◽  
Ventilation And Perfusion

Adequate gas exchange in the lungs requires a balance between three key processes: ventilation (V), the flow of gas from the environment to the alveoli; perfusion (Q), the circulation to the pulmonary capillary beds; and diffusion of the gas from the alveolar space into the alveolar capillaries. This chapter discusses the management of diseases of the air space, which include secretions, pneumonia, pulmonary edema, and hemoptysis. Collectively these conditions result in the build-up of fluid in the alveolar space and thickening of the alveolar membrane, leading to a mismatch in ventilation and perfusion (V/Q mismatch). Both anesthesia and disease states can adversely affect gas exchange and the chapter discusses strategies to maximize a patient’s pulmonary status in order to minimize perioperative pulmonary complications.

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