Physical determinants of bronchial mucosal folding

Lambert, Robert A.; Codd, Sarah L.; Alley, M.R.; Pack, R. J.

doi:10.1152/jappl.1994.77.3.1206

Cited by 121 publications

(98 citation statements)

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“…We assume that the bubble advances at a steady speed (U), leaving a thin film of liquid on the wall of the inflated section of tube. The tube in the physical model is assumed to remain axisymmetric, whereas a real airway may buckle into a nonaxisymmetric configuration when compressed (36). We bypass such geometric complications for the present by regarding physical quantities {such as the tube radius [R(x)], where x measures distance along the axis of the tube} as representative of the mean airway radius averaged around the tube cross section.…”

Section: Methodsmentioning

confidence: 99%

Transient elastohydrodynamic drag on a particle moving near a deformable wall

Weekley

Waters

Jensen

2006

The Quarterly Journal of Mechanics and Applied Mathematics

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Naire, Shailesh, and Oliver E. Jensen. Epithelial cell deformation during surfactant-mediated airway reopening: a theoretical model. J Appl Physiol 99: 458 -471, 2005. First published March 31, 2005 doi:10.1152/japplphysiol.00796.2004.-A theoretical model is presented describing the reopening by an advancing air bubble of an initially liquid-filled collapsed airway lined with deformable epithelial cells. The model integrates descriptions of flow-structure interaction (accounting for nonlinear deformation of the airway wall and viscous resistance of the airway liquid flow), surfactant transport around the bubble tip (incorporating physicochemical parameters appropriate for Infasurf), and cell deformation (due to stretching of the airway wall and airway liquid flows). It is shown how the pressure required to drive a bubble into a flooded airway, peeling apart the wet airway walls, can be reduced substantially by surfactant, although the effectiveness of Infasurf is limited by slow adsorption at high concentrations. The model demonstrates how the addition of surfactant can lead to the spontaneous reopening of a collapsed airway, depending on the degree of initial airway collapse. The effective elastic modulus of the epithelial layer is shown to be a key determinant of the relative magnitude of strains generated by flow-induced shear stresses and by airway wall stretch. The model also shows how epithelial-layer compressibility can mediate strains arising from flow-induced normal stresses and stress gradients. recruitment; atelectrauma; volutrauma; fluid-structure interaction; surface tension SUCCESSFUL RECRUITMENT OF liquid-filled airways is a process of fundamental importance in human respiration, from the first breath onward, and is critical in the treatment of conditions such as infant or acute respiratory distress syndrome (ARDS). It is of particular current interest in the context of ARDS, where atelectrauma [damage to airway epithelium through the repeated opening and closing of airways and alveoli (9, 13, 43)], volutrauma [airway overdistension (56, 58)], and biotrauma (inflammatory airway insult secondary to mechanical injury) are candidate mechanisms of ventilator-induced lung injury (49, 53). Mechanisms of atelectrauma, for example, involve processes interacting over widely varying length scales: at the scale of the whole lung (involving forced inflation of a heterogeneous airway network); at the scale of an individual airway (where surface tension, airway compliance, and airway liquid viscosity are significant); at the scale of an airway epithelial cell (deforming in response to its local mechanical environment); and at the scale of individual molecules (for example epithelial-cell mechanosensors such as stretchactivated ion channels). Mathematical and computational models provide powerful tools with which to integrate descriptions of processes operating across such disparate scales. This paper seeks to contribute to the development of a theoretical framework for airway recruitment and specifically aims ...

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Section: Methodsmentioning

confidence: 99%

Transient elastohydrodynamic drag on a particle moving near a deformable wall

Weekley

Waters

Jensen

2006

The Quarterly Journal of Mechanics and Applied Mathematics

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“…Airway remodelling is a well-documented phenomenon associated with asthma development. Thickening of some airway wall components seen in asthmatic airways may contribute to excessive airway narrowing [146]; thickening of other components may have a protective effect against excessive narrowing [147][148][149][150][151]. Many of these predictions were based on computer simulations of geometrical changes in airway components and, therefore, were limited by the assumptions associated with the simulation.…”

Section: Removal Of Smooth Muscle From Asthmatic Airwaysmentioning

confidence: 99%

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

An¹,

Bai²,

Bates³

et al. 2007

European Respiratory Journal

341

298

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Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma.As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling.Anti-inflammatory therapy, however, does not ''cure'' asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM.In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.

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“…Whether smooth muscle is able to shorten in vivo depends not only on smooth muscle force but also on the load on the shortening smooth muscle. On the one hand the load could be increased due to thickening and stiffening of the heavily inflamed inner airway wall area [38,39]. On the other hand, it could be reduced due to uncoupling of the smooth muscle from the tethering forces of the parenchyma [1].…”

Section: Airway Dimensions Airflow Obstruction and Bronchial Responsmentioning

confidence: 99%

Cartilaginous airway wall dimensions and airway resistance in cystic fibrosis lungs

Tiddens¹,

Koopman²,

Lambert³

et al. 2000

Eur Respir J

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It is not clear how airway pathology relates to the severity of airflow obstruction and increased bronchial responsiveness in cystic fibrosis (CF) patients. The aim of this study was to measure the airway dimensions of CF patients and to estimate the importance of these dimensions to airway resistance using a computational model.Airway dimensions were measured in lungs obtained from CF patients who had undergone lung transplantation (n=12), lobectomy (n=1), or autopsy (n=4). These dimensions were compared to those of airways from lobectomy specimens from 72 patients with various degrees of chronic obstructive pulmonary disease (COPD). The airway dimensions of the CF and COPD patients were introduced into a computational model to study their effect on airway resistance.The inner wall and smooth muscle areas of peripheral CF airways were increased 3.3-and 4.3-fold respectively compared to those of COPD airways. The epithelium was 53% greater in height in peripheral CF airways. The sensitivity and maximal plateau resistance of the computed dose/response curves were substantially increased in the CF patients compared to COPD patients.The changes in airway dimensions of cystic fibrosis patients probably contribute to the severe airflow obstruction, and to increased bronchial responsiveness, in these patients. Eur Respir J 2000; 15: 735±742.

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Physical determinants of bronchial mucosal folding

Cited by 121 publications

References 0 publications

Transient elastohydrodynamic drag on a particle moving near a deformable wall

Transient elastohydrodynamic drag on a particle moving near a deformable wall

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

Cartilaginous airway wall dimensions and airway resistance in cystic fibrosis lungs

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