کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2952294 1577423 2008 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function : Sustained Vascular Injury and Blunted Nitric Oxide Production
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Brief Secondhand Smoke Exposure Depresses Endothelial Progenitor Cells Activity and Endothelial Function : Sustained Vascular Injury and Blunted Nitric Oxide Production
چکیده انگلیسی

ObjectivesThis study sought to analyze the effects of acute secondhand smoke (SHS) exposure on the number and function of endothelial progenitor cells (EPCs) over 24 h.BackgroundSecondhand smoke increases the risk of vascular disease and is a major public health concern, but the mechanism(s) of action are not fully understood.MethodsHealthy nonsmokers (age SEM 30.3 ± 1.3 years, n = 10) were exposed to 30 min of SHS yielding cotinine levels commonly observed in passive smokers and to smokefree air on 2 separate days. Measurements were taken before exposure (baseline), immediately after (0 h), and at 1 h, 2.5 h, and 24 h after. The EPCs (CD133+/KDR+, CD34+/KDR+) and endothelial microparticles (EMPs: CD31+/CD41−, CD144+, CD62e+) were determined in blood using flow cytometry. The EPC chemotaxis toward vascular endothelial growth factor was measured. Endothelial function was assessed as flow-mediated dilation (FMD) using ultrasound.ResultsSecondhand smoke exposure increased EPCs and plasma vascular endothelial growth factor and completely abolished EPC chemotaxis during 24 h after exposure. Secondhand smoke increased EMPs and decreased FMD. Although FMD returned to baseline at 2.5 h, EMPs and vascular endothelial growth factor levels remained elevated at 24 h, suggesting endothelial activation and injury with functional impairment of the vascular endothelium. Exposure to smokefree air had no effect. Incubation of EPCs from nonexposed subjects with plasma isolated from SHS-exposed subjects in vitro decreased chemotaxis by blockade of vascular endothelial growth factor–stimulated nitric oxide production.ConclusionsBrief exposure to real-world levels of SHS leads to sustained vascular injury characterized by mobilization of dysfunctional EPCs with blocked nitric oxide production. Our results suggest that SHS not only affects the vascular endothelium, but also the function of EPCs.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the American College of Cardiology - Volume 51, Issue 18, 6 May 2008, Pages 1760–1771
نویسندگان
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