Acute Effects of Passive Smoking on Peripheral Vascular Function

Abstract

Abstract-Environmental tobacco smoke (ETS) acutely affects peripheral and coronary vascular tone. Whether ETS exerts specific deleterious effects on aortic wave reflection through nicotine exposure, whether they persist after ETS cessation, and whether the smoke environment impairs microvascular function and increases asymmetrical dimethyl-arginine levels are not known. We tested these hypotheses in a randomized, crossover study design in 11 healthy male nonsmokers. The effects of 1 hour of exposure to ETS, as compared with a nontobacco smoke and normal air, on augmentation index corrected for heart rate and skin microvascular hyperemia to local heating were examined. Augmentation index increased both during (Pϭ0.01) and after (PϽ0.01) the ETS session but remained unchanged in the nontobacco smoke session when compared with normal air. Nicotine levels after the exposure were related to the peak rise in augmentation index (rϭ0.84; PϽ0.01), denoting a predominant role of nicotine in ETS vascular effects. This was confirmed in a second set of experiments (nϭ14), where the sublingual administration of nicotine was associated with an acute impairment in wave reflection as compared with placebo (Pϭ0.001). Both ETS and nontobacco smokes increased plasma asymmetrical dimethyl-arginine levels (PϽ0.001), but only ETS reduced the late rise in skin blood flow in response to heating (Pϭ0.03). In conclusion, passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. However, both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels. Key Words: passive smoking Ⅲ nicotine Ⅲ endothelium Ⅲ wave reflection Ⅲ nitric oxide E xposure to environmental tobacco smoke (ETS) has been recognized recently as a strong contributor to cardiovascular mortality, accounting for Ͼ50 000 deaths annually in the United States. 1 In recent years, extensive research has elucidated many aspects of the long-term ETS-related adverse effects on the cardiovascular system. 1 However, the use of normal air inhalation as a control limits the interpretation of the physiopathological processes underlying the acute cardiovascular toxicity of ETS. [2][3][4] Whether lung irritation and/or the stress provoked by smoke inhalation generate a nonspecific cardiovascular reaction 5 and whether this can explain the effect of ETS 2-4 are not known. We, therefore, decided to test the hypothesis that the vascular effects of ETS cannot simply be ascribed to a nonspecific reaction to smoke. This would provide further clear-cut evidence that ETS exerts specific deleterious cardiovascular effects beyond those of smoke pollution.To further prove the specificity of the toxic effects of ETS, our second new hypothesis was that the deleterious vascular effects of ETS would be related to the rise in plasma nicotine levels. The above-mentioned studies 2-4 did not determine plasma nicotine. The role of nicotine in the changes ...

Using multifractal detrended fluctuation analysis to assess sacral skin blood flow oscillations in people with spinal cord injury

“…Warner et al showed that nicotine caused a decrease in resting and maximal skin blood flow responses to prolonged heating [44]. Argacha et al demonstrated that passive smoking was associated with a prolonged rise of skin blood flow in response to local heating [45]. We did not exclude smokers from this study.…”

Lead, Smoking, and Peripheral Vascular Function

“…We read with interest the article by Argacha et al 1 dealing with acute effects of passive smoking on peripheral vascular function. The authors presented data concluding that passive smoking specifically increases aortic wave reflection through a nicotinedependent pathway and impairs microvascular function, even after the end of the exposure.…”

“…Both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels. 1 It is well documented that exposure to environmental tobacco smoke is a strong contributor to cardiovascular mortality, accounting for Ͼ50 000 deaths annually in the United States. 2 In a recent study from Greece, a 12 times higher lead concentration was found in tobacco smokers than in nonsmokers living in the midaltitudes of the northern hemisphere.…”

Short Term Effects of Public Smoking Bans on Health

“…Both factors occur within 30 minutes after exposure to smoke and are both risk factors for AMI. A reduction in the number of AMIs is thus quantifiable immediately after the introduction of the smoking ban, being it evident starting from the initial days after the reduction of smoking exposure (Richiardi et al 2009;Argacha et al, 2008). This means that we can evaluate the short-term effect of this policy.…”