LUNG-TISSUE RESISTANCE AND HYSTERETIC MODULI OF LUNG PARENCHYMA

Citation
E. Kimmel et al., LUNG-TISSUE RESISTANCE AND HYSTERETIC MODULI OF LUNG PARENCHYMA, Journal of applied physiology, 79(2), 1995, pp. 461-466
Citations number
17
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
79
Issue
2
Year of publication
1995
Pages
461 - 466
Database
ISI
SICI code
8750-7587(1995)79:2<461:LRAHMO>2.0.ZU;2-H
Abstract
Lung tissue resistance (Rti) represents a large and labile component o f total pulmonary resistance, but the mechanism is unknown. One hypoth esis that has received some support in the literature is that on expos ure to contractile agonists airway smooth muscle shortens and then, by the agency of elastic interdependence, induces distortion in surround ing parenchyma. Parenchymal distortion induced in the vicinity of a co nstricted airway is a pure shear deformation, but currently there are no data available for shear hysteresivity. Guided by a microstructural model, we have assigned stiffness and hysteresivity to microstructura l elements and then computed how those properties are expressed at the macroscale in bulk hysteresivities for both shear and volumetric expa nsion. Hysteresivity for volumetric expansion is shown to be a stiffne ss-weighted average of hysteresivities of all microstructural componen ts. But as the hysteresivity of microstructural elements increases, th at for shear deformation increases to some degree but eventually attai ns a plateau. Blunted hysteretic response in shear seems to be an intr insic property of pressure-supported structures, like the lung, that r equire an inflating pressure to ensure mechanical stability. The analy sis indicates that that part of Rti attributable to parenchymal distor tion can be at most a small fraction of that attributable to volumetri c expansion. These results are purely theoretical in nature, and this suggests that caution is necessary in their interpretation. However, t he mechanical basis of the results is sufficiently general to conclude that the hypothesis that parenchymal distortion secondary to bronchoc onstriction can account for Rti and its changes seems to be implausibl e.