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Effect of cigarette smoking on hypercapnia induced shear‐mediated dilation in the internal carotid artery
Author(s) -
Suzuki Kazuya,
Washio Takuro,
Tsukamoto Shingo,
Kato Kazunori,
Iwamoto Erika,
Ogoh Shigehiko
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.688.2
Subject(s) - hypercapnia , medicine , internal carotid artery , cardiology , brachial artery , peripheral , endothelial dysfunction , middle cerebral artery , respiratory system , blood pressure , ischemia
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 .