Cigarette smoking has been associated with diminished vasodilatory function in the airway circulation. It is possible that cigarette smoking similarly affects the pulmonary circulation before resting pulmonary circulatory abnormalities manifest.
To compare in smokers and never-smokers the acute effect of inhaled albuterol on airway and pulmonary hemodynamic function, as an index of β2-adrenoceptor-mediated vasodilation.
In 30 adults, airway and pulmonary vascular function was assessed before and 15-min after albuterol inhalation (270 μg). From mean systemic arterial pressure (MAP), cardiac output, airway blood flow (Qaw), and mean pulmonary arterial pressure (MPAP), airway vascular resistance (AVR) and pulmonary vascular resistance (PVR) were derived.
Albuterol induced a substantial drop in mean (± SE) PVR (-67.2% ± 5%), with no difference between groups. In contrast, the albuterol-induced decrease in AVR was significantly greater in never-smokers than smokers (-28.6% ± 3% vs. -3.1% ± 6%; p < 0.02).
These results are consistent with a dysfunction within a β2-adrenergic signaling pathway mediating vasorelaxation in the airway circulation of current-smokers. The vasodilatory deficit in the airway but not the pulmonary circulation could be related to local differences in the impact of cigarette smoke on the vascular endothelium.