期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 118, 期 1, 页码 36-41出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00684.2014
关键词
airway-parenchymal interdependence; airway resistance; computational model; airway hyperresponsiveness
资金
- National Heart, Lung, and Blood Institute [R01 HL-103405]
- National Institute of General Medical Sciences [P30 GM-103532]
The pathogenesis of late-onset T(H)2-low asthma in obesity is thought to be related to weight-related decreases in lung volume, but why only a subset of individuals with obesity develop this condition is unknown. We tested the hypothesis that natural variations in both airway wall stiffness and airway wall thickness could lead to a subpopulation of hyperresponsive individuals exhibiting the symptoms of asthma in the setting of obesity. Increases in airway resistance (R-aw) after airway smooth muscle stimulation were simulated using a computational model of an elastic airway embedded in elastic parenchyma. Using a range of randomly chosen values for both airway wall stiffness and thickness, we determined the resulting probability distributions of R-aw responsiveness for a variety of different levels of transpulmonary pressure (P-tp). As P-tp decreased from 5 to 1 cmH(2)O, the resulting distributions of Raw moved toward progressively higher levels of responsiveness. With appropriate choices for the mean and standard deviation of the parameter that controls either airway wall stiffness or thickness, the model predicts a relationship between airway hyperresponsiveness and body mass index that is similar to that which has been reported in populations with obesity. We conclude that natural variations in airway wall mechanics and geometry between different individuals can potentially explain why an increasing percentage of the population exhibits the symptoms of asthma as the obesity of the population increases.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据