scholarly journals Tissue Elastance

2020 ◽  
Author(s):  
Keyword(s):  
Tissue Elastance

Time course of respiratory mechanics during histamine challenge in the dog

1992 ◽  
Vol 73 (6) ◽  
pp. 2643-2647 ◽  
Author(s):  
A. M. Lauzon ◽  
G. Dechman ◽  
J. H. Bates
Keyword(s):  
Time Course ◽  
Airway Resistance ◽  
Respiratory Mechanics ◽  
Smooth Muscles ◽  
Atropine Sulfate ◽  
Mechanical Parameters ◽  
Peripheral Airways ◽  
Tissue Resistance ◽  
Histamine Challenge ◽  
Tissue Elastance

We studied the dynamics of respiratory mechanical parameters in anesthetized tracheostomized paralyzed dogs challenged with a bolus of histamine injected either venously (venous group) or arterially (arterial group). The venous group was further divided into two groups: the first was bilaterally vagotomized and received hexamethonium bromide (denervated group), and the second also received atropine sulfate (atropine group). In the venous group, tissue resistance (Rti) and tissue elastance (Eti) increased biphasically, whereas airway resistance was monophasic and synchronized with the second rise of the tissue parameters. In the arterial group, Rti, Eti, and airway resistance increased synchronously. The denervated and atropine groups showed dynamics similar to those of the venous group. We postulate that the first phase observed in Rti and Eti in the venous group is due to constriction of the smooth muscles of the peripheral airways and blood vessels distorting the parenchyma. The second and larger phase is then due to histamine reaching the bronchial circulation and constricting the central airways, again distorting the parenchyma. The results from the arterial group support this hypothesis, whereas those from the denervated group ascertain that none of the phases observed in the venous group was due to nervous reflexes.

scholarly journals Tissue heterogeneity in the mouse lung: effects of elastase treatment

2004 ◽  
Vol 97 (1) ◽  
pp. 204-212 ◽  
Author(s):  
Satoru Ito ◽  
Edward P. Ingenito ◽  
Stephen P. Arold ◽  
Harikrishnan Parameswaran ◽  
Nora T. Tgavalekos ◽  
...  
Keyword(s):  
Airway Resistance ◽  
Compartment Model ◽  
Mouse Lung ◽  
Tissue Elasticity ◽  
Single Compartment Model ◽  
In Series ◽  
Four Levels ◽  
Fitting Error ◽  
Tissue Elastance ◽  
Tissue Element

We developed a network model in an attempt to characterize heterogeneity of tissue elasticity of the lung. The model includes a parallel set of pathways, each consisting of an airway resistance, an airway inertance, and a tissue element connected in series. The airway resistance, airway inertance, and the hysteresivity of the tissue elements were the same in each pathway, whereas the tissue elastance (H) followed a hyperbolic distribution between a minimum and maximum. To test the model, we measured the input impedance of the respiratory system of ventilated normal and emphysematous C57BL/6 mice in closed chest condition at four levels of positive end-expiratory pressures. Mild emphysema was developed by nebulized porcine pancreatic elastase (PPE) (30 IU/day × 6 days). Respiratory mechanics were studied 3 wk following the initial treatment. The model significantly improved the fitting error compared with a single-compartment model. The PPE treatment was associated with an increase in mean alveolar diameter and a decrease in minimum, maximum, and mean H. The coefficient of variation of H was significantly larger in emphysema (40%) than that in control (32%). These results indicate that PPE treatment resulted in increased time-constant inequalities associated with a wider distribution of H. The heterogeneity of alveolar size (diameters and area) was also larger in emphysema, suggesting that the model-based tissue elastance heterogeneity may reflect the underlying heterogeneity of the alveolar structure.

Tissue elastance influences airway smooth muscle shortening: comparison of mechanical properties among different species

2002 ◽  
Vol 80 (9) ◽  
pp. 865-871 ◽  
Author(s):  
Anabelle M. Opazo Saez ◽  
R Robert Schellenberg ◽  
Mara S Ludwig ◽  
Richard A Meiss ◽  
Peter D Paré
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Isometric Force ◽  
Published Data ◽  
Passive Tension ◽  
Active Force ◽  
Muscle Shortening ◽  
Human Airways ◽  
Tissue Elastance

We have observed striking differences in the mechanical properties of airway smooth muscle preparations among different species. In this study, we provide a novel analysis on the influence of tissue elastance on smooth muscle shortening using previously published data from our laboratory. We have found that isolated human airways exhibit substantial passive tension in contrast to airways from the dog and pig, which exhibit little passive tension (<5% of maximal active force versus ~60% for human bronchi). In the dog and pig, airway preparations shorten up to 70% from Lmax (the length at which maximal active force occurs), whereas human airways shorten by only ~12% from Lmax. Isolated airways from the rabbit exhibit relatively low passive tension (~22% Fmax) and shorten by 60% from Lmax. Morphologic evaluation of airway cross sections revealed that 25-35% of the airway wall is muscle in canine, porcine, and rabbit airways in contrast to ~9% in human airway preparations. We postulate that the large passive tension needed to stretch the muscle to Lmax reflects the high connective tissue content surrounding the smooth muscle, which limits shortening during smooth muscle contraction by imposing an elastic load, as well as by causing radial constraint.Key words: isometric force, isotonic shortening, elastance.

Inhibition of alveolarization and altered pulmonary mechanics in mice expressing GATA-6

2003 ◽  
Vol 285 (6) ◽  
pp. L1246-L1254 ◽  
Author(s):  
Cong Liu ◽  
Machiko Ikegami ◽  
Mildred T. Stahlman ◽  
Chitta R. Dey ◽  
Jeffrey A. Whitsett
Keyword(s):  
Epithelial Cells ◽  
Surfactant Protein ◽  
Mouse Lung ◽  
Pulmonary Mechanics ◽  
Respiratory Epithelial Cells ◽  
Surfactant Protein C ◽  
Spatial Regulation ◽  
Respiratory Epithelial ◽  
Tissue Elastance

GATA-6, a member of a family of zinc finger transcription factors, is expressed in epithelial cells of the developing lung. To further assess the role of GATA-6 in lung morphogenesis, GATA-6 was expressed in respiratory epithelial cells of the developing mouse lung under control of the surfactant protein C promoter (hSP-CGATA-6 mice). Although GATA-6 did not alter lung morphology at embryonic day 18.5, defects in alveolar septation were observed early in the neonatal period, and air space enlargement persisted to adulthood. Airway resistance, airway elastance, tissue damping, and tissue elastance were significantly decreased, and lung volumes were significantly increased at 12 wk of age. Normal postnatal morphogenesis of the lung depends upon precise temporal-spatial regulation of GATA-6.

The bimodal quasi-static and dynamic elastance of the murine lung

2008 ◽  
Vol 105 (2) ◽  
pp. 685-692 ◽  
Author(s):  
Graeme R. Zosky ◽  
Tibor Z. Janosi ◽  
Ágnes Adamicza ◽  
Elizabeth M. Bozanich ◽  
Vincenzo Cannizzaro ◽  
...  
Keyword(s):  
Lung Volume ◽  
Lung Mechanics ◽  
Mouse Lung ◽  
Forced Oscillation Technique ◽  
Mechanically Ventilated ◽  
Thoracic Gas Volume ◽  
Residual Capacity ◽  
Gas Volume ◽  
Tissue Elastance

The double sigmoidal nature of the mouse pressure-volume (PV) curve is well recognized but largely ignored. This study systematically examined the effect of inflating the mouse lung to 40 cm H2O transrespiratory pressure (Prs) in vivo. Adult BALB/c mice were anesthetized, tracheostomized, and mechanically ventilated. Thoracic gas volume was calculated using plethysmography and electrical stimulation of the intercostal muscles. Lung mechanics were tracked during inflation-deflation maneuvers using a modification of the forced oscillation technique. Inflation beyond 20 cm H2O caused a shift in subsequent PV curves with an increase in slope of the inflation limb and an increase in lung volume at 20 cm H2O. There was an overall decrease in tissue elastance and a fundamental change in its volume dependence. This apparent “softening” of the lung could be recovered by partial degassing of the lung or applying a negative transrespiratory pressure such that lung volume decreased below functional residual capacity. Allowing the lung to spontaneously recover revealed that the lung required ∼1 h of mechanical ventilation to return to the original state. We propose a number of possible mechanisms for these observations and suggest that they are most likely explained by the unfolding of alveolar septa and the subsequent redistribution of the fluid lining the alveoli at high transrespiratory pressure.

Nonuniform expansion of constricted dog lungs

1996 ◽  
Vol 80 (2) ◽  
pp. 522-530 ◽  
Author(s):  
R. D. Hubmayr ◽  
M. J. Hill ◽  
T. A. Wilson
Keyword(s):  
Airway Resistance ◽  
Lower Lobe ◽  
Lung Parenchyma ◽  
Frequency Dependent ◽  
Lung Capacity ◽  
Before And After ◽  
Radiopaque Markers ◽  
Video Fluoroscopy ◽  
Control State ◽  
Tissue Elastance

The parenchymal marker technique was used to measure regional tidal volumes of samples of lung parenchyma in four open-chest supine dogs. Radiopaque markers that had been implanted in the lower lobe were tracked by biplane video fluoroscopy during sinusoidal volume oscillations at tidal volumes of approximately 20% of total lung capacity and frequencies of 1-40 breaths/min before and after methacholine was administered by aerosol. The volumes of tetrahedrons with apexes at four markers were computed, and sine waves were fit to the data for volume vs. time for each tetrahedron. The ratio of mean regional volume to mean airway pressure decreased by 10-45% after exposure to methacholine. Dynamic lung elastance and resistance of the constricted lungs were larger than control, and both were frequency dependent. Regional elastance and resistance varied considerably among tetrahedrons, and these were also frequency dependent. The data were fit by a model in which tissue elastance was uniform and nearly equal to elastance in the control state, but small-airway resistance was high and variable. We conclude that the lung contracts under bronchoconstriction but that the increased dynamic elastance and resistance of the constricted lung may be primarily the result of nonuniform increased airway resistance at the level of the terminal bronchioles.

Airway and tissue mechanics in a murine model of asthma: alveolar capsule vs. forced oscillations

2002 ◽  
Vol 93 (1) ◽  
pp. 263-270 ◽  
Author(s):  
Shinichiro Tomioka ◽  
Jason H. T. Bates ◽  
Charles G. Irvin
Keyword(s):  
Airway Resistance ◽  
Forced Oscillation ◽  
Tissue Mechanics ◽  
Forced Oscillations ◽  
Control Group ◽  
Bronchial Responsiveness ◽  
Lung Elastance ◽  
Functional Consequences ◽  
Lung Periphery ◽  
Tissue Elastance

To better address the functional consequences of inflammation on bronchial responsiveness, we studied two groups of BALB/c mice: a nonimmunized control group ( n = 8) and a group immunized and challenged with inhaled ovalbumin ( n = 8). An alveolar capsule (AC) measured airway resistance (RawAC) and lung elastance (El). A forced oscillation (FO) technique independently estimated airway resistance (RawFO) and a parameter H ti related to tissue elastance. Ovalbumin-immunized and -challenged mice had increased numbers of eosinophils in bronchoalveolar lavage and increased responsiveness to methacholine (MCh). Corresponding parameters from the AC and FO techniques were correlated: RawAC vs. RawFO( r = 0.76) and El vs. H ti ( r = 0.88, P< 0.0001 in all cases). AC and FO techniques showed significant increases in tissue elastance in response to MCh but no significant increases in airway resistance. These results demonstrated that the AC and FO techniques yield essentially equivalent results in mice, even when the lung is inhomogeneous, and that the bronchoconstrictive responses to MCh and inflammation in mice are predominantly located in the lung periphery.

Size distribution of recruited alveolar volumes in airway reopening

2000 ◽  
Vol 89 (5) ◽  
pp. 2030-2040 ◽  
Author(s):  
Béla Suki ◽  
Adriano M. Alencar ◽  
József Tolnai ◽  
Tibor Asztalos ◽  
Ferenc Peták ◽  
...  
Keyword(s):  
Size Distribution ◽  
Total Lung Capacity ◽  
Transpulmonary Pressure ◽  
Wave Tube ◽  
Pressure Oscillations ◽  
Lung Capacity ◽  
Impedance Data ◽  
Tissue Elastance ◽  
Good Agreement ◽  
Lung Lobes

In 11 isolated dog lung lobes, we studied the size distribution of recruited alveolar volumes that become available for gas exchange during inflation from the collapsed state. Three catheters were wedged into 2-mm-diameter airways at total lung capacity. Small-amplitude pseudorandom pressure oscillations between 1 and 47 Hz were led into the catheters, and the input impedances of the regions subtended by the catheters were continuously recorded using a wave tube technique during inflation from −5 cmH2O transpulmonary pressure to total lung capacity. The impedance data were fit with a model to obtain regional tissue elastance (Eti) as a function of inflation. First, Eti was high and decreased in discrete jumps as more groups of alveoli were recruited. By assuming that the number of opened alveoli is inversely proportional to Eti, we calculated from the jumps in Eti the distribution of the discrete increments in the number of opened alveoli. This distribution was in good agreement with model simulations in which airways open in cascade or avalanches. Implications for mechanical ventilation may be found in these results.

Assessment of local lung impedance by the alveolar capsule oscillator in dogs: a model analysis

1996 ◽  
Vol 80 (4) ◽  
pp. 1165-1172 ◽  
Author(s):  
M. Mishima ◽  
Z. Balassy ◽  
J. H. Bates
Keyword(s):  
Computer Simulations ◽  
Acoustic Impedance ◽  
Airway Resistance ◽  
Lung Region ◽  
Bronchial Challenge ◽  
Airway Constriction ◽  
Branching Model ◽  
Peripheral Airway ◽  
Lung Periphery ◽  
Tissue Elastance

The alveolar capsule oscillator technique has shown that the response of the lung periphery to intravenous histamine injection in dogs is extremely inhomogeneous both in terms of local peripheral airway resistance (RA) and local peripheral elastance (EA) (M. Mishima, Z Balassy, and J. H. T. Bates. J. Appl. Physiol. 77: 2140-2148, 1994). To assess the physical extent of the local lung region identified by this technique, we performed computer simulations using an asymmetrical branching model of the canine lung proposed by K. Horsfield, W. Kemp, and S. Philips (J. Appl. Physiol. 52: 21-26, 1982). The acoustic impedance of the model from 26 to 200 Hz as seen from the alveolar capsule oscillator was calculated. RA and EA were estimated from the simulated acoustic impedance between 26 and 200 Hz and were found to be 492 hPa.s.l-1 and 156,300 hPa/l, respectively. These values are similar to those found experimentally in previous studies. By simulating data using the model in various stages of completeness, we determined that approximately 50% of RA is determined by the acinus to which the alveolar capsule is attached, whereas the remainder is determined by airways < or = 1 mm diameter that converge on this acinus. By contrast, EA was determined almost entirely (95%) by the acinus directly under the capsule. Inhomogeneous peripheral airway constriction altered RA severalfold but did not affect EA by >5%. This suggests that the previously observed changes induced in EA by bronchial challenge reflect real changes in intrinsic tissue elastance rather than merely regional mechanical inhomogeneities.

scholarly journals A role for decorin in a murine model of allergen-induced asthma

2011 ◽  
Vol 300 (6) ◽  
pp. L863-L873 ◽  
Author(s):  
Cinzia L. Marchica ◽  
Valentina Pinelli ◽  
Marcos Borges ◽  
Jaryd Zummer ◽  
Venkatesan Narayanan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Airway Resistance ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Complex Impedance ◽  
Transforming Growth Factor Β ◽  
Proliferation And Apoptosis ◽  
Airway Mechanics ◽  
Tissue Elastance

Decorin (Dcn) is an extracellular matrix proteoglycan, which affects airway mechanics, airway-parenchymal interdependence, airway smooth muscle proliferation and apoptosis, and transforming growth factor-β bioavailability. As Dcn deposition is differentially altered in asthma, we questioned whether Dcn deficiency would impact the development of allergen-induced asthma in a mouse model. Dcn−/− and Dcn+/+ mice (C57Bl/6) were sensitized with ovalbumin (OA) and challenged intranasally 3 days/wk × 3 wk. After OA challenge, mice were anesthetized, and respiratory mechanics measured under baseline conditions and after delivery of increasing concentrations of methacholine aerosol. Complex impedance was partitioned into airway resistance and tissue elastance and damping. Bronchoalveolar lavage was performed. Lungs were excised, and tissue sections evaluated for inflammatory cell influx, α-smooth muscle actin, collagen, biglycan, and Dcn deposition. Changes in TH-2 cytokine mRNA and protein were also measured. Airway resistance was increased in OA-challenged Dcn+/+ mice only ( P < 0.05), whereas tissue elastance and damping were increased in both OA-challenged Dcn+/+ and Dcn−/−, but more so in Dcn+/+ mice ( P < 0.001). Inflammation and collagen staining within the airway wall were increased with OA in Dcn+/+ only ( P < 0.001 and P < 0.01, respectively, vs. saline). IL-5 and IL-13 mRNA were increased in lung tissue of OA-challenged Dcn+/+ mice. Dcn deficiency resulted in more modest OA-induced hyperresponsiveness, evident at the level of the central airways and distal lung. Differences in physiology were accompanied by differences in inflammation and remodeling. These findings may be, in part, due to the well-described ability of Dcn to bind transforming growth factor-β and render it less bioavailable.

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