A model for mechanical structure of the alveolar duct

1982 ◽  
Vol 52 (4) ◽  
pp. 1064-1070 ◽  
Author(s):  
T. A. Wilson ◽  
H. Bachofen
Keyword(s):  
Surface Tension ◽  
Lung Volume ◽  
Published Data ◽  
Scanning Electron Micrographs ◽  
Fiber System ◽  
Lung Capacity ◽  
Alveolar Duct ◽  
Tissue System ◽  
Line Elements ◽  
Air Liquid Interface

The appearance of the microstructure of the lung as revealed in transmission and scanning electron micrographs of perfusion-fixed air- and saline-filled lungs suggests the following model for the structure of the alveolar duct. There are two networks of force-bearing elements. The first is an interdependent part of the peripheral connective tissue system that starts from the pleura and extends into the interlobar and interlobular fissures. At the sublobular level, its geometry is not yet fully clear. This network is extended by changes in lung volume and is insensitive to surface tension. The second network is composed of the line elements that form the rims of the alveolar openings. This network is the terminal part of the axial fiber system that surrounds bronchi, bronchioli, and arteries. The line elements of this network are extended by the outward force of surface tension. The two-dimensional alveolar walls that form the alveoli are negligible mechanical components except as platforms for surface tension at the air-liquid interface. An analysis of the mechanics of this model yields relations among surface area, recoil pressure, lung volume, and surface tension that are consistent with published data for lung volumes below 80% of total lung capacity.

Effect of surface tension on circulation in the excised lungs of dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 707-712 ◽  
Author(s):  
I. Bruderman ◽  
K. Somers ◽  
W. K. Hamilton ◽  
W. H. Tooley ◽  
J. Butler
Keyword(s):  
Surface Tension ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Lung Volume ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Pressure ◽  
Pulmonary Arterial ◽  
Air Liquid Interface ◽  
Effect Of Surface

The hypothesis that the surface tension of the fluid film which lines the lung alveoli reduces the pericapillary pressure in air-filled lungs was tested by perfusing the excised lungs of dogs with saline, 6% dextran in saline, and blood. After almost maximal inflation with air from low volumes or the degassed state (inflation state) the pulmonary arterial pressure, relative to the base of the lungs, was lower than the alveolar pressure with flows up to 50 ml/min. It was higher than the alveolar pressure at any flow when the air-liquid interface had been abolished by filling the lungs to the same volume with fluid. The pulmonary arterial pressure at the same flow and alveolar pressure was lower in the inflation state than after deflation from higher volumes (the deflation state). However, lung volume was larger in the deflation state. The possibility of some low resistance channels in the inflation state could not be excluded. However, histological examinations showed that the alveolar capillaries were patent and failed to show any airless lung. pulmonary circulation; pericapillary pressure in lungs; surface tension and pulmonary vascular resistance Submitted on July 29, 1963

The Mechanical Behavior of a Mammalian Lung Alveolar Duct Model

1995 ◽  
Vol 117 (3) ◽  
pp. 254-261 ◽  
Author(s):  
E. Denny ◽  
R. C. Schroter
Keyword(s):  
Experimental Data ◽  
Mechanical Properties ◽  
Collagen Fiber ◽  
Fiber Bundles ◽  
Published Data ◽  
The Finite Element Method ◽  
Dependent Relationship ◽  
Alveolar Duct ◽  
Mammalian Lung ◽  
Air Liquid Interface

A model for the mechanical properties of an alveolar duct is analyzed using the finite element method. Its geometry comprises an assemblage of truncated octahedral alveoli surrounding a longitudinal air duct. The amounts and distributions of elastin and collagen fiber bundles, modeled by separate stress-strain laws, are based upon published data for dogs. The surface tension of the air-liquid interface is modeled using an area-dependent relationship. Pressure-volume curves are computed that compare well with experimental data for both saline-filled and air-filled lungs. Pressure-volume curves of the separate elastin and collagen fiber contributions are similar in form to the behavior of saline-filled lungs treated with either elastase or collagenase. A comparison with our earlier model, based upon a single alveolus, shows the duct to have a behavior closer to reported experimental data.

Parenchymal mechanics, gas mixing, and the slope of phase III

2013 ◽  
Vol 115 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Theodore A. Wilson
Keyword(s):  
Surface Tension ◽  
Regional Differences ◽  
Phase Iii ◽  
Published Data ◽  
Gas Mixing ◽  
Elastic Line ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Regional Compliance ◽  
Line Elements

A model of parenchymal mechanics is revisited with the objective of investigating the differences in parenchymal microstructure that underlie the differences in regional compliance that are inferred from gas-mixing studies. The stiffness of the elastic line elements that lie along the free edges of alveoli and form the boundary of the lumen of the alveolar duct is the dominant determinant of parenchymal compliance. Differences in alveolar size cause parallel shifts of the pressure-volume curve, but have little effect on compliance. However, alveolar size also affects the relation between surface tension and pressure during the breathing cycle. Thus regional differences in alveolar size generate regional differences in surface tension, and these drive Marangoni surface flows that equilibrate surface tension between neighboring acini. Surface tension relaxation introduces phase differences in regional volume oscillations and a dependence of expired gas concentration on expired volume. A particular example of different parenchymal properties in two neighboring acini is described, and gas exchange in this model is calculated. The efficiency of mixing and slope of phase III for the model agree well with published data. This model constitutes a new hypothesis concerning the origin of phase III.

Relations among recoil pressure, surface area, and surface tension in the lung

1981 ◽  
Vol 50 (5) ◽  
pp. 921-930 ◽  
Author(s):  
T. A. Wilson
Keyword(s):  
Surface Tension ◽  
Surface Energy ◽  
Total Energy ◽  
Surface Area ◽  
Lung Volume ◽  
Mechanical Energy ◽  
Energy Difference ◽  
Published Data ◽  
Recoil Pressure ◽  
Pressure Surface

The difference between energy stored in air- and saline-filled lungs is the sum of surface energy and the energy of tissue distortion caused by surface tension. The surface energy is zeta gamma dS, where gamma is surface tension and S is surface area. There is no corresponding relation between tissue energy and measurable variables. However, two equations can be obtained from the expression for the total energy difference. One is the statement that the total energy of the lung is minimum at equilibrium, and the other is the statement of conservation of mechanical energy as lung volume changes. The expression for tissue energy is eliminated between the two equations to obtain a single relation among the variables of interest: recoil pressure, surface area, and surface tension. Published data on recoil pressure and surface area of saline-filled, air-filled, and detergent-washed rabbit lungs are used in these equations to determine surface tension as a function of lung volume. The values of surface tension deduced from this analysis are lower than the values that would be obtained if the additional tissue forces in the air-filled lung were neglected. The contribution of tissue forces to the added recoil of the air-filled lung increases with increasing lung volume and accounts for approximately half the additional recoil at high lung volume.

Viscoelastic Behavior of a Lung Alveolar Duct Model

1999 ◽  
Vol 122 (2) ◽  
pp. 143-151 ◽  
Author(s):  
E. Denny ◽  
R. C. Schroter
Keyword(s):  
Surface Tension ◽  
Tidal Volume ◽  
Viscoelastic Behavior ◽  
Surface Tension Force ◽  
Element Model ◽  
Lung Parenchyma ◽  
Oscillatory Behavior ◽  
Published Data ◽  
Elastic Model ◽  
Alveolar Duct

A study is conducted into the oscillatory behavior of a finite element model of an alveolar duct. Its load-bearing components consist of a network of elastin and collagen fibers and surface tension acting over the air–liquid interfaces. The tissue is simulated using a visco-elastic model involving nonlinear quasi-static stress–strain behavior combined with a reduced relaxation function. The surface tension force is simulated with a time- and area-dependent model of surfactant behavior. The model was used to simulate lung parenchyma under three surface tension cases: air-filled, liquid-filled, and lavaged with 3-dimethyl siloxane, which has a constant surface tension of 16 dyn/cm. The dynamic elastance Edyn and tissue resistance Rti were computed for sinusoidal tidal volume oscillations over a range of frequencies from 0.16–2.0 Hz. A comparison of the variation of Edyn and Rti with frequency between the model and published experimental data showed good qualitative agreement. Little difference was found in the model between Rti for the air-filled and lavaged models; in contrast, published data revealed a significantly higher value of Rti in the lavaged lung. The absence of a significant increase in Rti for the lavaged model can be attributed to only minor changes in the individual fiber bundle resistances with changes in their configuration. The surface tension was found to make an important contribution to both Edyn and Rti in the air-filled duct model. It was also found to amplify any existing tissue dissipative properties, despite exhibiting none itself over the small tidal volume cycles examined. [S0148-0731(00)00502-1]

Tracing surfactant transformation from cellular release to insertion into an air-liquid interface

2004 ◽  
Vol 286 (5) ◽  
pp. L1009-L1015 ◽  
Author(s):  
T. Haller ◽  
P. Dietl ◽  
H. Stockner ◽  
M. Frick ◽  
N. Mair ◽  
...  
Keyword(s):  
Surface Tension ◽  
Cultured Cells ◽  
High Surface ◽  
Lamellar Body ◽  
Liquid Interface ◽  
Alveolar Type ◽  
Tensile Forces ◽  
Modify Surface ◽  
Fluorescence Imaging Microscopy ◽  
Air Liquid Interface

Pulmonary surfactant is secreted by alveolar type II cells as lipid-rich, densely packed lamellar body-like particles (LBPs). The particulate nature of released LBPs might be the result of structural and/or thermodynamic forces. Thus mechanisms must exist that promote their transformation into functional units. To further define these mechanisms, we developed methods to follow LBPs from their release by cultured cells to insertion in an air-liquid interface. When released, LBPs underwent structural transformation, but did not disperse, and typically preserved a spherical appearance for days. Nevertheless, they were able to modify surface tension and exhibited high surface activity when measured with a capillary surfactometer. When LBPs inserted in an air-liquid interface were analyzed by fluorescence imaging microscopy, they showed remarkable structural transformations. These events were instantaneous but came to a halt when the interface was already occupied by previously transformed material or when surface tension was already low. These results suggest that the driving force for LBP transformation is determined by cohesive and tensile forces acting on these particles. They further suggest that transformation of LBPs is a self-regulated interfacial process that most likely does not require structural intermediates or enzymatic activation.

Rib cage and abdominal restrictions have different effects on lung mechanics

1980 ◽  
Vol 49 (6) ◽  
pp. 946-952 ◽  
Author(s):  
C. A. Bradley ◽  
N. R. Anthonisen
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Lung Mechanics ◽  
Elastic Recoil ◽  
Rib Cage ◽  
Lung Capacity ◽  
Single Breath ◽  
Restrictive Procedures ◽  
Maximum Expiratory Flow ◽  
Per Se

The effects of a variety of restrictive procedures on lung mechanics were studied in eight healthy subjects. Rib cage restriction decreased total lung capacity (TLC) by 43% and significantly increased elastic recoil and maximum expiratory flow (MEF). Subsequent immersion of four subjects with rib cage restriction resulted in no further change in either parameter; shifts of blood volume did not reverse recoil changes during rib cage restriction. Abdominal restriction decreased TLC by 40% and increased MEF and elastic recoil, but recoil was increased significantly less than was the case with rib cage restriction. Further, at a given recoil pressure, MEF was less during rib cage restriction than during either abdominal restriction or no restriction. Measurements of the unevenness of inspired gas distribution by the single-breath nitrogen technique showed increased unevenness during rib cage restriction, which was significantly greater than that during abdominal restriction. We conclude that lung volume restriction induces changes in lung function, but the nature of these changes depends on how the restriction is applied and therefore cannot be ascribed to low lung volume breathing per se.

Airway surface liquid thickness as a function of lung volume in small airways of the guinea pig

1994 ◽  
Vol 77 (5) ◽  
pp. 2333-2340 ◽  
Author(s):  
D. Yager ◽  
T. Cloutier ◽  
H. Feldman ◽  
J. Bastacky ◽  
J. M. Drazen ◽  
...  
Keyword(s):  
Surface Tension ◽  
Epithelial Cells ◽  
Guinea Pig ◽  
Cross Sections ◽  
Lung Volume ◽  
Longitudinal Direction ◽  
Small Airways ◽  
Airway Surface Liquid ◽  
Residual Capacity ◽  
Surface Liquid

The average thickness and distribution of airway surface liquid (ASL) on the luminal surface of peripheral airways were measured in normal guinea pig lungs frozen at functional residual capacity (FRC) and total lung capacity (TLC). Tissue blocks containing cross sections of airways of internal perimeter 0.188–3.342 mm were cut from frozen lungs and imaged by low-temperature scanning electron microscopy (LTSEM). Measurements made from LTSEM images were found to be independent of freezing rate by comparison of measurements at rapid and slow freezing rates. At both lung volumes, the ASL was not uniformly distributed in either the circumferential or longitudinal direction; there were regions of ASL where its thickness was < 0.1 micron, whereas in other regions ASL collected in pools. Discernible liquid on the surfaces of airways frozen at FRC followed the contours of epithelial cells and collected in pockets formed by neighboring cells, a geometry consistent with a low value of surface tension at the air-liquid interface. At TLC airway liquid collected to cover epithelial cells and to form a liquid meniscus, a geometry consistent with a higher value of surface tension. The average ASL thickness (h) was approximately proportional to the square root of airway internal perimeter, regardless of lung volume. For airways of internal perimeter 250 and 1,800 microns, h was 0.9 and 1.8 microns at FRC and 1.7 and 3.7 microns at TLC, respectively. For a given airway internal perimeter, h was 1.99 times thicker at TLC than at FRC; the difference was statistically significant (P < 0.01; 95% confidence interval 1.29–3.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Inspiratory muscles during exercise: a problem of supply and demand

1988 ◽  
Vol 64 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
P. Leblanc ◽  
E. Summers ◽  
M. D. Inman ◽  
N. L. Jones ◽  
E. J. Campbell ◽  
...  
Keyword(s):  
Lung Volume ◽  
Static Pressure ◽  
Total Lung Capacity ◽  
Supply And Demand ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Maximum Exercise ◽  
Lung Capacity ◽  
Inspiratory Muscles ◽  
Residual Capacity

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.

Effects of surface tension and intraluminal fluid on mechanics of small airways

1997 ◽  
Vol 82 (1) ◽  
pp. 233-239 ◽  
Author(s):  
Mark J. Hill ◽  
Theodore A. Wilson ◽  
Rodney K. Lambert
Keyword(s):  
Surface Tension ◽  
Bending Stiffness ◽  
Liquid Interface ◽  
Cross Sectional Area ◽  
Pressure Curve ◽  
Small Airways ◽  
Sectional Area ◽  
Cross Sectional ◽  
Inner Surface ◽  
Air Liquid Interface

Hill, Mark J., Theodore A. Wilson, and Rodney K. Lambert.Effects of surface tension and intraluminal fluid on the mechanics of small airways. J. Appl. Physiol.82(1): 233–239, 1997.—Airway constriction is accompanied by folding of the mucosa to form ridges that run axially along the inner surface of the airways. The muscosa has been modeled (R. K. Lambert. J. Appl. Physiol. 71: 666–673, 1991) as a thin elastic layer with a finite bending stiffness, and the contribution of its bending stiffness to airway elastance has been computed. In this study, we extend that work by including surface tension and intraluminal fluid in the model. With surface tension, the pressure on the inner surface of the elastic mucosa is modified by the pressure difference across the air-liquid interface. As folds form in the mucosa, intraluminal fluid collects in pools in the depressions formed by the folds, and the curvature of the air-liquid interface becomes nonuniform. If the amount of intraluminal fluid is small, <2% of luminal volume, the pools of intraluminal fluid are small, the air-liquid interface nearly coincides with the surface of the mucosa, and the area of the air-liquid interface remains constant as airway cross-sectional area decreases. In that case, surface energy is independent of airway area, and surface tension has no effect on airway mechanics. If the amount of intraluminal fluid is >2%, the area of the air-liquid interface decreases as airway cross-sectional area decreases, and surface tension contributes to airway compression. The model predicts that surface tension plus intraluminal fluid can cause an instability in the area-pressure curve of small airways. This instability provides a mechanism for abrupt airway closure and abrupt reopening at a higher opening pressure.

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