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Modeling the resistance to airflow in the human lung Wiggs, Barry James Ryder
Abstract
To examine the influence of airway smooth muscle shortening and airway wall thickness on pulmonary resistance a model of the tracheobronchial tree has been developed which allows simulations of these mechanisms of airway narrowing. The model is based on both a symmetrical branching system proposed by Weibel (61) and an asymmetric branching scheme developed by Horsfield(21). Fluid mechanic equations proposed by Pedley (49) are used to calculate inspiratory resistance and to allow for changes in lung inflation the pressure area curves described by Lambert(32) are used. The model is easily implemented using a spreadsheet and personal computer which allows calculation of total and regional pulmonary resistance. At each generation or order in the model provision is made for the airway wall thickness, the maximal airway smooth muscle shortening achievable and an S shaped dose response relationship to describe the smooth muscle shortening. Measurements of airway wall thickness from 23 normal subjects whom died suddenly and 19 asthmatic subjects whom died of complications of their disease are related to internal airway perimeter using an iterative restricted maximum likelihood technique. Using the estimated relationship for airway wall thickness it is possible to partition the changes to central or peripheral airways. It is concluded that the model provides a realistic qualitative estimate of the tracheobronchial pressure drop that may provide valuable insights into the interaction of airway smooth muscle shortening and airway wall thickness as important contributors to airway hyperresponsiveness.
Item Metadata
Title |
Modeling the resistance to airflow in the human lung
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1989
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Description |
To examine the influence of airway smooth muscle shortening and airway wall thickness on pulmonary resistance a model of the tracheobronchial tree has been developed which allows simulations of these mechanisms of airway narrowing. The model is based on both a symmetrical branching system proposed by Weibel (61) and an asymmetric branching scheme developed by Horsfield(21). Fluid mechanic equations proposed by Pedley (49) are used to calculate inspiratory resistance and to allow for changes in lung inflation the pressure area curves described by Lambert(32) are used. The model is easily implemented using a spreadsheet and personal computer which allows calculation of total and regional pulmonary resistance. At each generation or order in the model provision is made for the airway wall thickness, the maximal airway smooth muscle shortening achievable and an S shaped dose response relationship to describe the smooth muscle shortening.
Measurements of airway wall thickness from 23 normal subjects whom died suddenly and 19 asthmatic subjects whom died of complications of their disease are related to internal airway perimeter using an iterative restricted maximum likelihood technique. Using the estimated relationship for airway wall thickness it is possible to partition the changes to central or peripheral airways.
It is concluded that the model provides a realistic qualitative estimate of the tracheobronchial pressure drop that may provide valuable insights into the interaction of airway smooth muscle shortening and airway wall thickness as important contributors to airway hyperresponsiveness.
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Genre | |
Type | |
Language |
eng
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Date Available |
2010-08-25
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0076959
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
1989-11
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Item Media
Item Citations and Data
Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.