Journal
JOURNAL OF CARDIOLOGY
Volume 56, Issue 3, Pages 307-313Publisher
ELSEVIER
DOI: 10.1016/j.jjcc.2010.07.003
Keywords
Smoking; Flow-mediated vasodilation; Plasminogen activator inhibitor type 1; Nitric oxide; Endothelium
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The aim of this study was to elucidate endothelial dysfunction due to chronic cigarette smoking in young smokers and to determine practical markers of the functional derangement. The subjects were young, healthy, mate non-smokers (n=11) and smokers (n=9). Endothelium-dependent and -independent vasodilation was assessed by flow-mediated vasodilation (FMD) and nitroglycerine-induced vasodilation (NID), respectively, and possible markers of endothelial function were measured. FMD in smokers was significantly lower than in control subjects (5.0 +/- 2.6% and 9.5 +/- 5.2%, p < 0.05). Plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator levels were significantly (p < 0.05) higher in smokers (6.7 +/- 4.5 ng/ml and 4.3 +/- 2.0 ng/ml) compared with control subjects (2.9 +/- 1.9 ng/ml and 3.0 +/- 0.6 ng/ml). Furthermore, PAI-1 levels correlated inversely with FMD (r= -0.451, p<0.05). No significant differences were observed for NID, or plasma NO2-, NOx, thrombomodulin, von Willebrand factor, and tissue factor pathway inhibitor levels. Chronic cigarette smoking-induced endothelial dysfunction and the PAI-1 level could be a good marker of endothelial dysfunction in young smokers. (C) 2010 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.
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