• Barry E Hurwitz, Eliana S Mendes, Andreas Schmid, Meela Parker, Johana Arana, Alex Gonzalez, and Adam Wanner.
• Behavioral Medicine Research Center, Miller School of Medicine, University of Miami, Coral Gables, FL; Division of Endocrinology, Diabetes, and Metabolism, Miller School of Medicine, University of Miami, Coral Gables, FL; Department of Psychology, University of Miami, Coral Gables, FL. Electronic address: bhurwitz@miami.edu.
• Chest. 2017 Mar 1; 151 (3): 650-657.

BackgroundCigarette 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 become manifested. The aim of this study was to compare the acute effect of inhaled albuterol on airway and pulmonary hemodynamic function as an index of β2-adrenoceptor-mediated vasodilation in smokers and never smokers.MethodsIn 30 adults, airway and pulmonary vascular function was assessed before and 15 min after albuterol inhalation (270 μg). From mean systemic arterial pressure, cardiac output, airway blood flow, and mean pulmonary arterial pressure, airway vascular resistance (AVR) and pulmonary vascular resistance (PVR) were derived.ResultsAlbuterol 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 in smokers (-28.6% ± 3% vs -3.1% ± 6%; P < .02).ConclusionsThese results are consistent with a dysfunction in a β2-adrenergic signaling pathway mediating vasorelaxation in the airway circulation of current smokers. The vasodilatory deficit in the airway circulation but not in the pulmonary circulation could be related to local differences in the impact of cigarette smoke on the vascular endothelium.Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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