Mechanisms Underlying Cerebrovascular Effects of Cigarette Smoking in Rats In Vivo

Abstract

Background and Purpose-The effects of acute smoking on cerebral circulation are controversial. This study was designed(1) to clarify any differences between the effects of cigarette smoking and nicotine infusion and between the effects of single-and multiple-cigarette smoking on cerebral vessels and (2) to probe the mechanism(s) underlying the vascular responses. Methods-In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, pial vessel diameters were measured with the use of a cranial window preparation. We studied the effects of (1) 60 puffs per minute of mainstream cigarette smoke from cigarettes having 2 nicotine levels (0.1 and 1 mg per cigarette), (2) administration of nicotine (0.05 mg per body IV), and (3) repeated smoking (four 1 mg nicotine-containing cigarettes at 30-minute intervals) (nϭ6 each). Results-Inhalation of smoke from a 0.1 or 1 mg nicotine-containing cigarette for 1 minute caused pial arterioles to constrict at 30 seconds (7.2% and 7.3%, respectively) and then to dilate (peak at 5 to 10 minutes; 4.6% and 17.9%, respectively). Nicotine infusion caused pial vasodilation (35.7%) without an initial vasoconstriction. Repeated smoking suppressed the pial vasodilation but not the initial vasoconstriction. The vasodilation induced by a single cigarette was greatly inhibited by pretreatment with mecamylamine or glibenclamide and attenuated by propranolol or N -nitro-Larginine methyl ester; the initial vasoconstriction was inhibited by seratrodast, a thromboxane A 2 receptor antagonist (nϭ6 in each case). Conclusions-Single-cigarette smoking had a significant biphasic effect on cerebral arteriolar tone. The vasodilation was attenuated by repeated smoking. The vasodilation is most likely an effect of nicotine, at least in part mediated via sympathetic activation, NO production, and K ϩ channel activation. The vasoconstriction is partially due to thromboxane A 2 induced by cigarette smoke. (Stroke. 1998;29:1656-1665.)

Smoking and choroidal thickness in patients over 65 with early-atrophic age-related macular degeneration and normals

“…(a) One-way analysis of variance (ANOVA) between lifetime nonsmokers, current smokers, and former smokers; green diamonds vertically centered on mean spanning 1 SD; horizontal width proportional to sample size; mean CT as follows: nonsmokers, 181±65, n ¼ 80; current smokers, 147±61, n ¼ 10; former smokers, 149 ± 64 mm, n ¼ 57; P ¼ 0.011; (b) Two-sample t-test subgroup analysis of patients with drusen or early AMD; mean CT is as follows: nonsmokers, 146 ± 46 mm, n ¼ 49; history of smoking, 121 ± 41 mm, n ¼ 49; P ¼ 0.006. exposure. 41 Smoking appears to impair endothelial cell function in many vascular regions, and evidence supports long-term vasoconstriction and altered endothelial response 37,42,43 to various vasoactive mediators in tobacco smoke. 40,44,45 Human studies indicate abnormal choroidal vascular reactivity to carbogen (high oxygen) inhalation in chronic smokers.…”

Changes in Cardio-Ankle Vascular Index in Smoking Cessation

“…In addition, large amounts of free radicals in cigarette smoke lower the activation of nitrogen monoxide, which in turn may obstruct the vasodilatation reaction in vascular wall cells. These are some of the examples of the many proposed mechanisms of cigarette smoke toxicity [23][24][25][26][27][28][29] . Unlike other arteriosclerotic risk factors, these acute actions by nicotine show rapid emergence upon smoking and rapid alleviation upon cessation of smoking.…”

Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for KCa, KATP, and KVchannels, nitric oxide, and prostanoids

“…However, it remains to be determined if K Ca channels are also important in the regulation of nicotinic cutaneous vasodilation. Further, ATP-sensitive K + (K ATP ) channels reportedly contribute to nicotinic vasodilation as evidenced in thoracic aortae and pial arterioles of rats (Iida et al 1998; Zou D r a f t Mechanisms of nicotinic skin vasodilation and sweating 4 et al 2012). However, the extent to which K ATP channels may play a role in mediating nicotinic cutaneous vasodilation and sweating is unknown.…”