Abstract
In the present study, we hypothesized that habitual cigarette smoking attenuates endothelial function in the cerebral circulation as well as that of the peripheral circulation in young adults. To test this hypothesis, we measured cerebrovascular and peripheral flow‐mediated dilation (FMD) in young smokers and nonsmokers in the present study. Ten healthy nonsmokers and 10 smokers participated in the study. We measured blood velocity and diameter in the brachial artery and internal carotid artery (ICA) using Doppler ultrasound. We identified shear‐mediated dilation in the brachial artery and ICA by the percentage change in peak diameter during hyperemia stimulation (reactive hyperemia and hypercapnia). We measured the baseline diameter and the shear rate area under the curve from the onset of hyperemia to peak dilation in the brachial artery and ICA, finding the measurements of the smokers and those of the nonsmokers did not differ (p > .05). In contrast to brachial FMD (5.07 ± 1.79% vs. 7.92 ± 3.01%; smokers vs. nonsmokers, p = .019), FMD in the ICA was not attenuated in the smokers compared with that of the nonsmokers (5.46 ± 2.32% vs. 4.57 ± 2.70%; p = .442). These findings indicate that in young healthy smokers, cerebral endothelial function was preserved, and the response of cerebral endothelial function to smoking was different from that of peripheral vasculature.
Highlights
Habitual cigarette smoking is well known to cause hypertension (Virdis, Giannarelli, Neves, Taddei, & Ghiadoni, 2010), lung damage (Vial, 1986), dysfunction of peripheral vascular function (Ambrose & Barua, 2004), and subsequent impairment of systemic vascular function
In contrast to our hypothesis, cerebrovascular (ICA) flow-mediated dilation (FMD) in smokers was not different from that of nonsmokers. These findings indicate that cerebral endothelial function was preserved in young healthy smokers, and that the response of cerebral endothelial function to smoking was different from that of peripheral vasculature
Peripheral FMD was significantly lower in smokers than that in nonsmokers (Figure 2), indicating that peripheral endothelial function was attenuated in young healthy smokers
Summary
Habitual cigarette smoking is well known to cause hypertension (Virdis, Giannarelli, Neves, Taddei, & Ghiadoni, 2010), lung damage (Vial, 1986), dysfunction of peripheral vascular function (Ambrose & Barua, 2004), and subsequent impairment of systemic vascular function. Other studies (Silvestrini, Troisi, Matteis, Cupini, & Bernardi, 1996; Terborg, Birkner, et al, 2002) reported that cerebrovascular reactivity to hypercapnia was reduced after cigarette smoking These findings suggest that this acute negative effect of smoking a cigarette on cerebral hemodynamics could contribute partly to the increased risk of cerebral infarction in current smokers. It has been suggested that the transcranial Doppler data they used may be reflected by smoking-induced vasoconstriction of the isolated vessel (Terborg, Bramer, et al, 2002) Both the effects of habitual cigarette smoking on cerebral circulation and the physiological mechanism triggering the onset of cerebrovascular diseases in smokers remain unclear
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