• Hiroki Iida, Mami Iida, Motoyasu Takenaka, Naokazu Fukuoka, and Shuji Dohi.
• Department of Anesthesiology and Pain Medicine, Gifu University Graduate School of Medicine, Gifu-City, Gifu, Japan. iida@gifu-u.ac.jp
• J. Thromb. Thrombolysis. 2010 May 1;29(4):483-8.

AbstractWe previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that a reduction of oxidative stress by agents such as valsartan, fasudil, or apocynin prevented this impairment. Here, our aim was to investigate the comparative effects of two antiplatelet drugs used for stroke-prevention [a phosphodiesterase-3 inhibitor (cilostazol) and a cyclooxygenase inhibitor (aspirin)] on smoking-induced endothelial dysfunction in cerebral arterioles. In Sprague-Dawley rats, we used a closed cranial window preparation to measure the changes in pial vessel diameters induced by topical application of acetylcholine (ACh) following intraperitoneal injection of 0.5% carboxymethyl cellulose sodium salt (CMC; vehicle control for the antiplatelet drugs). After 1-min smoking (1 mg-nicotine cigarette), the arteriolar responses to ACh were reexamined. Finally, after intraperitoneal cilostazol or aspirin (each in 0.5% CMC) pretreatment, we reexamined the vasodilator responses to topical ACh (before and after cigarette smoking). Under control conditions, cerebral arterioles were dose-relatedly dilated by topical ACh (10(-6) and 10(-5 )M). One hour after 1-min smoking, 10(-5 )M ACh (a) constricted cerebral pial arterioles in the control group and in the aspirin-pretreatment group (responses not significantly different from each other), but (b) dilated cerebral pial arteries in the cilostazol pretreatment groups (responses significantly different from those obtained without cilostazol pretreatment). Thus, cilostazol (but not aspirin) may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.

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