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.

It has been well established that chronic cigarette smoking causes peripheral endothelial dysfunction which is strongly associated with coronary and peripheral vascular diseases. Thus, smoking is a risk factor for these diseases. On the other hand, some previous studies suggest that smoking is also a risk factor for cerebral vascular disease. However, its physiological mechanism remains unknown. Under these backgrounds, we hypothesized that smoking also attenuated cerebral endothelial function. To test this hypothesis, we measured shear‐mediated dilation in the internal carotid artery (ICA) as an index of cerebral endothelial function in smokers and non‐smokers. The subject were young, healthy, male non‐smokers (n=6, age 21.2±0.8 years, BMI 21.3±4.1) and smokers (n=5, 21.8±1.6 years, BMI 19.5±1.8). Each smoker consumed an average of 9 cigarettes per day (range 6–10). Shear‐mediated dilation in the ICA was measured by using Doppler ultrasound. Shear‐mediated dilation in the ICA was induced for 3 min during inspiration of high carbon dioxide concentration gas (target end‐tidal carbon dioxide; +10mmHg from individual baseline value) and it was calculated as the percent rise in peak diameter during hypercapnia stimulation from baseline value. As a result, there was no difference in both baseline diameter and blood velocity of the ICA between smokers and non‐smokers (diameter, 4.39 ± 0.54 mm vs 4.87 ± 0.65 mm, P = 0.22; blood velocity, 35.2 ± 8.1 cm/s vs 32.7 ± 6.3 cm/s, P = 0.57). Similarly, shear‐mediated dilation in the ICA was not affected by habitual smoking (smokers vs. non‐smokers; 4.53 ± 2.34 % vs 2.23 ± 3.36 %, P = 0.23), indicating that the effect of chronic smoking on cerebrovascular endothelial function may be minimal in this age group. The findings of the present study suggest that the influence of chronic smoking on endothelial function in the brain is different from that of the peripheral vasculature.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.