• Adam Wanner, Michael A Campos, and Eliana Mendes.
• Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Miami Miller School of Medicine, P.O. Box 016960 (R-47), Miami, FL 33101, USA. awanner@miami.edu
• Pulm Pharmacol Ther. 2007 Jan 1;20(2):126-9.

AbstractCigarette smoking has been associated with impaired endothelium-dependent relaxation responses in the brachial and coronary arteries (endothelial dysfunction). The aim of the present study was to determine if the airway circulation is also affected and if airway treatment has an effect on endothelial function. Airway blood flow (Q(aw)) responses to inhaled albuterol as an index of endothelial function were measured in age-matched healthy current smokers, healthy ex-smokers, ex-smokers with COPD and healthy lifetime non-smokers; in the ex-smokers with COPD, the albuterol responsiveness was repeated after a 4-week treatment with an inhaled glucocorticoid/beta(2)-adrenergic agonist combination drug. Mean baseline Q(aw) was similar in the four groups. Albuterol inhalation increased mean Q(aw) in lifetime non-smokers (50.1+/-8.3%; p<0.05) and in healthy ex-smokers (37.2+/-3.4%; p<0.05) but not in healthy current smokers (13.9+/-3.2%; p=NS) and ex-smokers with COPD (9.7+/-4.5%; p=NS). While drug treatment per se did not change Q(aw) significantly, it restored albuterol responsiveness (+67.6+/-11.1%; p<0.05) in the ex-smokers with COPD. Thus, cigarette smoking is associated with endothelial dysfunction in the airway, with a partial recovery of endothelial function after smoking cessation in healthy ex-smokers but not in ex-smokers with COPD. In the latter, combined glucocorticoid/beta(2)-adrenergic agonist treatment restores albuterol responsiveness.

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