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Original Research: Tobacco Cessation and Prevention |

Airway and Pulmonary β2-Adrenergic Vasodilatory Function in Current Smokers and Never Smokers

Barry E. Hurwitz, PhD; Eliana S. Mendes, MD; Andreas Schmid, MD; Meela Parker, RDCS; Johana Arana, MA; Alex Gonzalez, BA; Adam Wanner, MD
Author and Funding Information

FUNDING/SUPPORT: This study was supported by an academic grant from GlaxoSmithKline [117259].

aBehavioral Medicine Research Center, Miller School of Medicine, University of Miami, Coral Gables, FL

bDivision of Endocrinology, Diabetes, and Metabolism, Miller School of Medicine, University of Miami, Coral Gables, FL

cDivision of Pulmonary, Critical Care, and Sleep Medicine, Miller School of Medicine, University of Miami, Coral Gables, FL

dDepartment of Psychology, University of Miami, Coral Gables, FL

CORRESPONDENCE TO: Barry E. Hurwitz, PhD, Behavioral Medicine, Clinical Physiology and Echocardiography Laboratory, Behavioral Medicine Research Center, University of Miami, Soffer Clinical Research Bldg No. 777, 1120 NW 14th St, Miami, FL 33136


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(3):650-657. doi:10.1016/j.chest.2016.12.008
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Background  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 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.

Methods  In 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.

Results  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 in smokers (–28.6% ± 3% vs –3.1% ± 6%; P < .02).

Conclusions  These 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.

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