Airway vascular endothelial function in healthy smokers without systemic endothelial dysfunction

Eliana Mendes, Jose Eduardo D Cancado, Patricia Rebolledo, Joahna Arana, Meela Parker, Alex Gonzalez, Barry Hurwitz, Adam Wanner

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background: Cigarette smoking can lead to systemic endothelial dysfunction. Since the airway circulation is exposed to a high concentration of cigarette smoke constituents, we reasoned that airway vascular endothelial dysfunction could be present in healthy smokers without systemic endothelial dysfunction. Objectives: The purpose of this study was to compare airway and systemic endothelial function and measure markers of systemic inflammation in lung-healthy current smokers. Since endothelial dysfunction in smokers has been related to systemic inflammation, we also investigated its response to an inhaled glucocorticosteroid (ICS). Methods: Fifteen healthy, current smokers and 17 healthy, lifetime nonsmokers were enrolled. Smokers were randomly assigned to 3-week treatments with inhaled fluticasone propionate or placebo in a crossover design. Vascular endothelial function was assessed in the airway by the airway blood-flow response to inhaled albuterol (ΔQaw) and in the extrapulmonary circulation by brachial arterial flow-mediated vasodilation (FMD). Venous blood was collected for C-reactive protein and IL-6. Results: Baseline parameters did not differ between groups except for ΔQaw, which was greater in nonsmokers (45% ± 12%) than smokers (1% ± 12%) (P=.001). In the smokers, ICS treatment increased Qaw to 41% ± 7% (P<.001), but had no effect on FMD or inflammatory markers. There was an inverse relationship between baseline and ICS-induced changes in ΔQaw. Conclusions: Healthy smokers with no signs of systemic inflammation or endothelial dysfunction display impaired airway vascular endothelial function, possibly preceding systemic endothelial dysfunction. Airway endothelial function was restored with an ICS, and the response was directly related to the severity of endothelial dysfunction.

Original languageEnglish
Pages (from-to)1733-1739
Number of pages7
JournalChest
Volume143
Issue number6
DOIs
StatePublished - Jun 1 2013

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Blood Vessels
Vasodilation
Inflammation
Albuterol
Smoke
Tobacco Products
C-Reactive Protein
Cross-Over Studies
Interleukin-6
Pneumonia
Arm
Smoking
Placebos
Therapeutics
Fluticasone

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Airway vascular endothelial function in healthy smokers without systemic endothelial dysfunction. / Mendes, Eliana; Cancado, Jose Eduardo D; Rebolledo, Patricia; Arana, Joahna; Parker, Meela; Gonzalez, Alex; Hurwitz, Barry; Wanner, Adam.

In: Chest, Vol. 143, No. 6, 01.06.2013, p. 1733-1739.

Research output: Contribution to journalArticle

Mendes E, Cancado JED, Rebolledo P, Arana J, Parker M, Gonzalez A et al. Airway vascular endothelial function in healthy smokers without systemic endothelial dysfunction. Chest. 2013 Jun 1;143(6):1733-1739. https://doi.org/10.1378/chest.12-1033
Mendes, Eliana ; Cancado, Jose Eduardo D ; Rebolledo, Patricia ; Arana, Joahna ; Parker, Meela ; Gonzalez, Alex ; Hurwitz, Barry ; Wanner, Adam. / Airway vascular endothelial function in healthy smokers without systemic endothelial dysfunction. In: Chest. 2013 ; Vol. 143, No. 6. pp. 1733-1739.
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N2 - Background: Cigarette smoking can lead to systemic endothelial dysfunction. Since the airway circulation is exposed to a high concentration of cigarette smoke constituents, we reasoned that airway vascular endothelial dysfunction could be present in healthy smokers without systemic endothelial dysfunction. Objectives: The purpose of this study was to compare airway and systemic endothelial function and measure markers of systemic inflammation in lung-healthy current smokers. Since endothelial dysfunction in smokers has been related to systemic inflammation, we also investigated its response to an inhaled glucocorticosteroid (ICS). Methods: Fifteen healthy, current smokers and 17 healthy, lifetime nonsmokers were enrolled. Smokers were randomly assigned to 3-week treatments with inhaled fluticasone propionate or placebo in a crossover design. Vascular endothelial function was assessed in the airway by the airway blood-flow response to inhaled albuterol (ΔQaw) and in the extrapulmonary circulation by brachial arterial flow-mediated vasodilation (FMD). Venous blood was collected for C-reactive protein and IL-6. Results: Baseline parameters did not differ between groups except for ΔQaw, which was greater in nonsmokers (45% ± 12%) than smokers (1% ± 12%) (P=.001). In the smokers, ICS treatment increased Qaw to 41% ± 7% (P<.001), but had no effect on FMD or inflammatory markers. There was an inverse relationship between baseline and ICS-induced changes in ΔQaw. Conclusions: Healthy smokers with no signs of systemic inflammation or endothelial dysfunction display impaired airway vascular endothelial function, possibly preceding systemic endothelial dysfunction. Airway endothelial function was restored with an ICS, and the response was directly related to the severity of endothelial dysfunction.

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