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Biomedical subjects

R K Lambert

Publications and source records attributed to R K Lambert.

At least 19 recordsLinked to original sources
PubMed1997

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

Airway constriction is accompanied by folding of the mucosa to form ridges that run axially along the inner surface of the airways. The mucosa 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.

Airway Resistance↗
PubMed1997

Lung parenchymal shear modulus, airway wall remodeling, and bronchial hyperresponsiveness.

When airways narrow, either through the action of smooth muscle shortening or during forced expiration, the lung parenchyma is locally distorted and provides an increased peribronchial stress that resists the narrowing. Although this interdependence has been well studied, the quantitative significance of airway remodeling to interdependence has not been elucidated. We have used an improved computational model of the bronchial response to smooth muscle agonists to investigate the relationships between airway narrowing (as indicated by airway resistance), parenchymal shear modulus, adventitial thickening, and inner wall thickening at lung recoil pressures of 4, 5, and 8 cmH2O. We have found that, at low recoil pressures, decreases in parenchymal shear modulus have a significant effect that is comparable to that of moderate thickening of the airway wall. At higher lung recoil pressures, the effect is negligible.

Airway Resistance↗
PubMed1995

Determinants of airway smooth muscle shortening in excised canine lobes.

There is marked heterogeneity of airway narrowing in intraparenchymal airways in response to bronchoconstricting stimuli. We hypothesized that this heterogeneity results from variations in the structure of the airway wall. Freshly excised dog lung lobes were inflated to transpulmonary pressures (PL) of between 5 and 15 cmH2O, and an aerosol containing a high concentration of carbachol was administered. The lobes were fixed and processed for light-microscopic examination and morphometric analysis of membranous airway dimensions. The relationships of smooth muscle shortening to PL and airway dimensions were analyzed using multiple linear regression. The results show that airway smooth muscle shortening was greater at lower PL and in airways with larger internal perimeter and a greater number of folds per internal perimeter and that it was less in airways with greater inner wall area. We conclude that the magnitude and variability of airway smooth muscle shortening and airway narrowing in response to maximal constricting stimuli are influenced by mechanical factors related to airway wall geometry.

Airway Resistance↗
PubMed1994

Tensile stiffness of ovine tracheal wall.

The epithelial folding that occurs during bronchoconstriction requires that the pressure on the muscle side of the folding membrane be greater than that on the lumen side. The pressure required for a given level of folding depends on the elastic properties of the tissue and on the geometry of the folding. To quantify the elastic properties, uniaxial tensile stiffness of the tracheal inner wall of nine sheep was measured in two directions: parallel to the tracheal axis and circumferentially. The tissue showed anisotropic behavior, being approximately three times stiffer longitudinally than circumferentially. Histological examination showed that collagen in the lamina propria was randomly arranged, whereas there were straight elastin fibers aligned with the tracheal axis. This observation could explain the observed elastic anisotropy. Mechanical removal of the epithelium had no effect on tensile stiffness. It was also found that the tissue was under tension in situ. When a strip was excised, its length decreased by > or = 30%. After allowing for the systematic errors inherent in this experiment, the in situ circumferential tensile stiffness is estimated to be > or = 20 kPa. If the equivalent tissue in the bronchioles has the same tensile stiffness as that in the trachea, the forces required to fold the membrane are significant at small transbronchial pressure differences and increase in the presence of membrane thickening such as that seen in asthma.

Animals↗
PubMed1994

Proposed nomenclature for quantifying subdivisions of the bronchial wall.

There is increasing interest in the structural components of the airway wall because of the airway remodeling that is observed in conditions such as asthma and chronic obstructive pulmonary disease and because of their contribution to changes in airway mechanics. This interest has stimulated several groups to make morphometric measurements on airway cross sections, and their results have been reported using a variety of nomenclature. We propose the adoption of a standard system of nomenclature that is based on accepted terms for subdivisions of the airway wall and has been agreed to by several groups working in this field.

Bronchi↗
PubMed1994

Physical determinants of bronchial mucosal folding.

It has recently been proposed, on the basis of a theoretical analysis, that the folding of the mucosa provides a significant component of airway stiffness. The model predicted that the stiffness of an airway was directly related to the number of epithelial folds that developed. In this study we examine the possibility that the folding pattern is determined by the physical requirements that the folding membrane must stay within the boundary of the smooth muscle wall, that the submucosal mass is constant, and that the strain energy of the folding membrane is the minimum possible within the geometric constraints. Model predictions are compared with morphometric data from the noncartilaginous airways of 17 sheep lungs. The data are in agreement with our predictions, which are based on the assumption that the folding membrane thickness is proportional to the submucosal thickness (in a fully dilated airway). The outcome of this analysis is that the increase in intrinsic stiffness of the folding membrane resulting from the increased thickness outweighs the decrease in stiffness conferred by the fewer folds required by the thicker submucosa. It is suggested that the increase in folding membrane thickness observed in asthma could be viewed as a protective mechanism that tends to reduce hyperresponsiveness.

Animals↗
PubMed1993

Functional significance of increased airway smooth muscle in asthma and COPD.

Using a computational model, we investigated the effect of the morphologically determined increased airway smooth muscle mass, adventitial mass, and submucosal mass observed in patients with asthma and chronic obstructive pulmonary disease (COPD) on the increase in airway resistance in response to a bronchoconstricting stimulus. The computational model of Wiggs et al. (J. Appl. Physiol. 69: 849-860, 1990) was modified in such a way that smooth muscle shortening was limited by the maximal stress that the muscle could develop at the constricted length. Increased adventitial thickness was found to increase constriction by reducing parenchymal interdependence. Increased submucosal thickness led to greater luminal occlusion for any degree of smooth muscle shortening. Increased muscle thickness allowed greater smooth muscle shortening against the elastic loads provided by parenchymal interdependence and airway wall stiffness. We found that for constant airway mechanics, as reflected by the passive area-pressure curves of the airways, the increased muscle mass is likely to be the most important abnormality responsible for the increased resistance observed in response to bronchoconstricting stimuli in asthma and COPD. For a given maximal muscle stress, greater muscle thickness allows the development of greater tension and thus more constriction of the lumen.

Adult↗
PubMed1991

A method for estimating the Young's modulus of complete tracheal cartilage rings.

Cartilage is primarily responsible for maintaining the stability of the large airways; yet very little is known about the mechanical properties of airway cartilage. This work establishes a technique whereby average values for the equilibrium modulus of excised tracheal cartilage rings can be obtained. An apparatus was designed to apply preset deformations to a tracheal segment and to monitor the deforming force. Segments of four human tracheae obtained postmortem and containing three rings were mounted in the apparatus after being stripped of posterior membrane. The load-deformation behavior was analyzed with a model on the basis of thin curved beam theory. Agreement between predicted deformed shapes and those observed was good in three of the four cases and in the case of a short length of longitudinally split rubber tube. The technique is suitable for comparing mechanical properties of cartilage before and after an intervention.

Biomechanical Phenomena↗
PubMed1991

Role of bronchial basement membrane in airway collapse.

Bronchial basement membrane is an elastic structure that has the potential to be load bearing and thus to contribute to the mechanical stiffness of the bronchus. To investigate this possible role, the membrane was modeled as a thin-walled linearly elastic tube surrounded by a uniform liquid on the outside and by air on the inside. When the external pressure on such a tube exceeds the internal pressure by a critical amount, the tube buckles reversibly into two or more folds. The critical buckling pressure varies as the square of the number of folds. The analysis was used to investigate the collapse behavior of the model tube into patterns ranging from 2 to 24 folds. This showed that the resistance to collapse increases rapidly as the number of folds increases. Data in the literature lead to the conclusion that the pressures involved in collapsing the tubes are probably in the physiological range. It is suggested, on the basis of the model results reported here, that bronchial hyperresponsiveness could be related to the number of folds into which the basement membrane buckles when the bronchial muscle contracts. A reduced number of folds would yield an increased response.

Air Pressure↗
PubMed1990

Simulation of the effects of mechanical nonhomogeneities on expiratory flow from human lungs.

A computational model for expiration from lungs with mechanical nonhomogeneities was used to investigate the effect of such nonhomogeneities on the distribution of expiratory flow and the development of alveolar pressure differences between regions. The nonhomogeneities used were a modest constriction of the peripheral airways and a 50% difference in compliance between regions. The model contains only two mechanically different regions but allows these to be as grossly distributed as left lung-right lung or to be distributed as a set of identical pairs of parallel nonhomogeneous regions with flows from each merging in a specified bronchial generation. The site of flow merging had no effect on the flow-volume curve but had a significant effect on the development of alveolar pressure differences (delta PA). With the peripheral constriction, greater values of delta PA developed when flows were merged peripherally rather than centrally. The opposite was true in the case of a compliance nonhomogeneity. The delta PA values were smaller at submaximal flows. Plots of delta PA vs. lung volume were similar to those obtained experimentally. These results were interpreted in terms of the expression used for the fluid mechanics of the merging flows. delta PA was greater when the viscosity of the expired gas was increased or when its density was reduced. Partial forced expirations were shown to indicate the presence of mechanical nonhomogeneity.

Forced Expiratory Flow Rates↗
PubMed1989

A new computational model for expiratory flow from nonhomogeneous human lungs.

A model has been developed for expiration from human lungs in which the mechanical properties of the airways and parenchyma can be varied between regions. The model is based on an existing homogeneous model. The fluid mechanical problem of the merging of dissimilar flows from adjacent regions is underspecified by the conservation laws of mass and energy. An existing, empirically derived result, provides the required extra equation. Model simulation of a nonhomogeneously distributed mild constriction of the peripheral airways gives results for maximal flows and alveolar pressure differences which are in good agreement with recent experimental findings.

Forced Expiratory Flow Rates↗
PubMed1988

In vitro tracheal mechanics by nuclear magnetic resonance imaging.

Images of rabbit tracheal cross sections were obtained at a series of transmural pressures ranging from 22 to -95 cmH2O by use of a nuclear magnetic resonance imaging microscope. The excised, washed tracheas were immersed in a solution of phosphate-buffered saline made up in deuterium oxide (D2O, pH 7.3). The images are maps of proton density in the image slice (2.5 mm thick). All but one series of images showed a collapse process in which the trachealis muscle invaginated asymmetrically, i.e., the muscle appeared to favor one side of the cartilage ring system more than the other. The connecting tissue between the cartilage rings appeared to be more compliant than the rings themselves, thus suggesting that the tracheal lumen became corrugated at negative pressures. In the plane of a cartilage ring, the lumen appeared to remain patent at pressures as low as -95 cmH2O. However, between rings, where the tracheal wall was more compliant, the lumen appeared to be totally occluded at -53 cmH2O. Lumen areas in both the plane of the cartilage rings and in a plane between rings were measured from each series of printed images for six tracheas. These measurements, when normalized, averaged, and plotted against transmural pressure gave asymptotic logarithmic compliances (n1 in the model of Lambert et al., J. Appl. Physiol. 52: 44-56, 1982) of 1.2 +/- 0.4 and 20 +/- 7 for the interring and ring regions, respectively. These values are greater than the critical value of 0.5 (J. Appl. Physiol. 62: 2426-2435, 1987) and are thus consistent with wave speed flow limitation being possible anywhere in the trachea during forced expiration.

Animals↗
PubMed1987

Removal of observer variability from the determination of the volume of isoflow.

The initial attractiveness of the volume of isoflow (VisoV) as an index of early small airways dysfunction has faded, perhaps because of VisoV's high variability, a significant part of which is contributed by the observer. We suggest here that the observer variability can be removed by filtering the flow data in the reciprocal volume domain, by using a modified foreign gas mixture in which some of the helium is replaced by neon, and by reading VisoV from a plot of density dependence vs. lung inflation. Support for these suggestions is drawn from both model simulations and experiments. Model simulations suggested that VisoV would be increased by the substitution of neon for some of the helium in the usual helium-oxygen (Helox) mixture. This was confirmed in tests on matched groups of normal and asymptomatic asthmatic children. The inclusion of 20% neon (Heneox20) was found to reduce the coefficient of variation in the mean value of VisoV in both groups of subjects. An interesting result of this test was that VisoV using Heneox20 was significantly higher in the asthmatic group than in the normal group, whereas VisoV using Helox was not. The results for density dependence (DD) between the 2 groups were not significantly different using Heneox20 but were using Helox. Plots of DD (derived from heavily filtered flow curves) vs. lung inflation showed an unambiguous value for VisoV.

Adolescent↗
PubMed1987

Bronchial mechanical properties and maximal expiratory flows.

Flow limitation in a collapsible elastic tube is dependent on the area (A) vs. pressure (P) relationship (the "tube law") for the tube. In this paper, a tube law in which A varies as (1-P)-n1 at negative pressures is assumed. It is shown that wave-speed limitation is possible at negative pressures only if n1 is greater than 0.5. Dissipative limitation is also investigated. Viscous limitation can occur if n1 is greater than 0.5, and turbulent limitation can occur if n1 is not less than 0.4. For values of n1 less than 0.4, flow cannot be limited at negative pressures. Model simulations are used to show that a combination of a value of n1 less than 0.3 together with an area minimum in the bronchial tree produce a minimum (a "hook") in the flow-volume curve. In the vicinity of such hooks, density dependence exceeds the usually accepted theoretical maximum value. Simulations also show that, when n1 is sufficiently small, apparently supramaximal flows appear to be possible.

Bronchi↗
PubMed1986

Analysis of bronchial mechanics and density dependence of maximal expiratory flow.

The computational model for expiratory flow in humans of Lambert and associates (J. Appl. Physiol. Respirat. Environ. Exercise Physiol. 52: 44-56, 1982) was used to investigate the effect of bronchial constrictions in three airway zones on the density dependence of maximal expiratory flow. It was found that constriction of the peripheral airways (less than 2 mm diam) reduced density dependence and increased the volume of isoflow. Constriction of the larger intraparenchymal airways resulted in increased density dependence at low lung volumes and essentially normal values at other volumes. The volume of isoflow was reduced. Extraparenchymal (but intrathoracic) airway constriction caused no change in the volume of isoflow but caused increased density dependence at the higher lung volumes. It was shown that in these model simulations the addition of extraparenchymal constriction to intraparenchymal constriction causes essentially no changes in density dependence. An increased volume of isoflow and significantly decreased density dependence at 50 and 25% vital capacity were produced by simulated constrictions only in the peripheral airways.

Biomechanical Phenomena↗
PubMed1984

Sensitivity and specificity of the computational model for maximal expiratory flow.

The computational model for forced expiratory flow from human lungs of Lambert and associates (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 44-56, 1982) was used to investigate the sensitivity of maximal expiratory flow to lung properties. It was found that maximal flow is very sensitive to recoil pressure and airway areas but not very sensitive to lung volume, airway compliance, and airway length. Linear programming was used to show that a given air flow-pressure curves was compatible with a fairly wide range of airway properties. Additional data for maximal flow with a He-O2 mixture narrowed the range somewhat. It was shown that the flow-pressure curve contains more information about central than peripheral airways and that information about the latter is obtainable only from flows at recoils less than 2 cmH2O. Parameter ranges compatible with individual flow-pressure curves showed differences that demonstrated that such curves give some indication of individual central airway properties.

Airway Resistance↗
PubMed1982

A computational model for expiratory flow.

A mathematical model of maximal expiratory flow was developed. Coupled equations describing the pressure losses in the flow and the pressure-area behavior of the airway were integrated along the airway from the periphery to the flow-limiting site. Equations describing pressure losses in the flow were adapted from studied of bronchial casts. The bronchial anatomy utilized was that described by Weibel. Bronchial mechanical properties were obtained from measurements in excised human lungs for the central airways and by extrapolations of these data for the peripheral airways. The maximal flow for air and helium predicted by the model agrees with that of five lungs from which mechanical properties were obtained. The model predictions agree with published values of density and viscosity dependence of maximal flow. At high and midlung volumes, maximal flow is determined primarily by the wave-speed mechanism. At low lung volumes, maximal flow is primarily determined by the coupling of viscous pressure losses and airway mechanical properties.

Biomechanical Phenomena↗