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Original Research |

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

Conflict of Interest Statement: A.W. has received investigator-initiated grants from GlaxoSmithKline, Merck, and AstraZeneca. He serves on the scientific advisory board of Aradigm Corp. E.S.M. has received an academic grant from AstraZeneca. The remaining authors have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Funding/Support: This study was supported by an academic grant from GlaxoSmithKline (117259).

1Behavioral Medicine Research Center, Miller School of Medicine, University of Miami, Miami, Florida, 33136 USA

2Department of Psychology, University of Miami, Coral Gables, Florida, 33124 USA

3Division of Endocrinology, Diabetes and Metabolism, Miller School of Medicine, University of Miami, Miami, Florida, 33136 USA

4Division of Pulmonary, Critical Care and Sleep Medicine, Miller School of Medicine, University of Miami, Miami, Florida, 33136 USA

Address correspondence to: Barry E. Hurwitz, Ph.D., Behavioral Medicine, Clinical Physiology & Echocardiography Laboratory, Behavioral Medicine Research Center, University of Miami, Clinical Research Building #777, 1120 NW 14th Street, Miami, FL 33136.


Copyright 2016, . All Rights Reserved.


Chest. 2016. doi:10.1016/j.chest.2016.12.008
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Abstract

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 manifest.

Objectives  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.

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 (MAP), cardiac output, airway blood flow (Qaw), and mean pulmonary arterial pressure (MPAP), 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 smokers (-28.6% ± 3% vs. -3.1% ± 6%; p < 0.02).

Conclusions  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.


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