| 1. |
- Wagers, S, et al.
(författare)
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Nonlinearity of respiratory mechanics during bronchoconstriction in mice with airway inflammation
- 2002
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Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 92:5, s. 1802-1807
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Tidskriftsartikel (refereegranskat)abstract
- Respiratory system resistance (R) and elastance (E) are commonly estimated by fitting the linear equation of motion P = EV + R(V) over dot + P-0 (Eq. 1) to measurements of respiratory pressure (P), lung volume (V), and flow (V). However, the respiratory system is unlikely to behave linearly under many circumstances. We determined the importance of respiratory system nonlinearities in two groups of mechanically ventilated Balb/c mice [controls and mice with allergically inflamed airways (ova/ova)], by,g the impact of the addition of nonlinear terms (E2V2 assessing and R-2(V) over dot (V) over dot) on the goodness of model fit seen with Eq. 1. Significant improvement in fit (51.85 +/- 4.19%) was on seen in the ova/ova mice during bronchoconstriction when the E2V2 alone was added. An improvement was also observed with addition of the E2V2 term in mice with both low and high lung volumes ventilated at baseline, suggesting a volume-dependent nonlinearity of E. We speculate that airway closure in the constricted ova/ova mice accentuated the volume-dependent nonlinearity by decreasing lung volume and overdistending the remaining lung.
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| 2. |
- Wagers, S, et al.
(författare)
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The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?
- 2004
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Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 96:6, s. 2019-2027
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Tidskriftsartikel (refereegranskat)abstract
- Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we show that the hyperresponsiveness of mice with allergically inflamed airways can be explained entirely by a thickening of the airway mucosa and an increased propensity of the airways to close, without the involvement of any increase in the degree of airway smooth muscle shortening. This has implications for the pathophysiology of asthma and suggests that at least some types of asthma may benefit from therapies aimed at manipulating surface tension at the air-liquid interface in the lungs.
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