WoundReference improves clinical decisions
 Choose the role that best describes you
Adams T, Wan E, Wei Y, Wahab R, Castagna F, Wang G, Emin M, Russo C, Homma S, Le Jemtel TH, Jelic S, et al.
Chest. Date of publication 2015 Jul 1;volume 148(1):112-119.
1. Chest. 2015 Jul;148(1):112-119. doi: 10.1378/chest.14-2045. Secondhand Smoking Is Associated With Vascular Inflammation. Adams T(1), Wan E(2), Wei Y(3), Wahab R(1), Castagna F(1), Wang G(1), Emin M(1), Russo C(2), Homma S(2), Le Jemtel TH(4), Jelic S(1). Author information: (1)Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NY. (2)Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY. (3)Division of Biostatistics, Columbia University College of Physicians and Surgeons, New York, NY. (4)Section of Cardiology, Tulane University School of Medicine, New Orleans, LA. Comment in Chest. 2015 Jul;148(1):6-8. BACKGROUND: The relative risk for cardiovascular diseases in passive smokers is similar to that of active smokers despite almost a 100-fold lower dose of inhaled cigarette smoke. However, the mechanisms underlying the surprising susceptibility of the vascular tissue to the toxins in secondhand smoke (SHS) have not been directly investigated. The aim of this study was to investigate directly vascular endothelial cell function in passive smokers. METHODS: Using a minimally invasive method of endothelial biopsy, we investigated directly the vascular endothelium in 23 healthy passive smokers, 25 healthy active smokers, and 23 healthy control subjects who had never smoked and had no regular exposure to SHS. Endothelial nitric oxide synthase (eNOS) function (expression of basal eNOS and activated eNOS [phosphorylated eNOS at serine1177 (P-eNOS)]) and expression of markers of inflammation (nuclear factor-κB [NF-κB]) and oxidative stress (nitrotyrosine) were assessed in freshly harvested venous endothelial cells by quantitative immunofluorescence. RESULTS: Expression of eNOS and P-eNOS was similarly reduced and expression of NF-κB was similarly increased in passive and active smokers compared with control subjects. Expression of nitrotyrosine was greater in active smokers than control subjects and similar in passive and active smokers. Brachial artery flow-mediated dilation was similarly reduced in passive and active smokers compared with control subjects, consistent with reduced endothelial NO bioavailability. CONCLUSIONS: Secondhand smoking increases vascular endothelial inflammation and reduces active eNOS to a similar extent as active cigarette smoking, indicating direct toxic effects of SHS on the vasculature. DOI: 10.1378/chest.14-2045 PMCID: PMC4493867 PMID: 25742439 [Indexed for MEDLINE]
Appears in following Topics:
Arterial Ulcer - Introduction and Assessment
How to Assess a Patient with Chronic Wounds