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1 Vermont Lung Center, Pulmonary and Critical Care Medicine, Department of Medicine, University of Vermont College of Medicine, Burlington, United States
2 Department of Medicine, University of Vermont College of Medciine, Vermont Lung Center, Pulmonary and Critical Care Medicine, Burlington, Vermont, United States
* To whom correspondence should be addressed. E-mail: charles.irvin{at}uvm.edu.
Aiway hyperresponsiveness (AHR) is a defining feature of asthma. We have previously shown, in mice sensitized and challenged with antigen, that AHR is attributable to normal airway smooth muscle contraction with exaggerated airway closure. In the current study we sought to determine if the same was true for mice known to have intrinsic AHR, the genetic strain of mice, A/J. We found that A/J mice have AHR characterized by minimal increase in elastance following aerosolized methacholine challenge compared to mice (BALB/c) that have been antigen sensitized and challenged (A/J PC50 22.9 ± 5.7 vs. 3.3 ± 0.4 mg/ml for antigen challenged and sensitized mice p<0.004). Similar results were found when intravenous methacholine was used (A/J PC30 0.22 ± 0.08 vs. 0.03 ± 0.004 mg/ml for antigen challenged and sensitized mice). Computational model analysis revealed that the AHR in A/J mice is dominated by exaggerated airway smooth muscle contraction and that when the route of methacholine administration was changed to intravenous, central airway constriction dominates. Absorption atelectasis was used to provide evidence of the lack of airway closure in A/J mice. Bronchoconstriction during ventilation with 100% oxygen resulted in a mean 9.8% loss of visible lung area in A/J mice compared to 28% in antigen sensitized and challenged mice (p<0.02). We conclude that the physiology of AHR depends upon the mouse model used and the route of bronchial agonist administration.
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