Effects of central airway shunting on the mechanical impedance of the mouse lung.

The mechanical properties of the lung are embodied in its mechanical input impedance, which it is interpreted in physiological terms by being fit with a mathematical model. The normal lung is extremely well described by a model consisting of a single uniformly ventilated compartment comprised of tissue having a constant-phase impedance, but to describe the abnormal lung it frequently becomes necessary to invoke additional compartments. To date, all evidence of regional mechanical heterogeneity in the mouse lung has been assumed to be of the parallel variety.

Inhaled salmeterol and/or fluticasone alters structure/function in a murine model of allergic airways disease.

Background: The relationship between airway structural changes (remodeling) and airways hyperresponsiveness (AHR) is unclear. Asthma guidelines suggest treating persistent asthma with inhaled corticosteroids and long acting beta-agonists (LABA). We examined the link between physiological function and structural changes following treatment fluticasone and salmeterol separately or in combination in a mouse model of allergic asthma.

Intrinsic and antigen-induced airway hyperresponsiveness are the result of diverse physiological mechanisms.

Airway 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 present study we sought to determine if the same was true for mice known to have intrinsic AHR, the genetic strain of mice, A/J.