Iida M, Iida H, Dohi S, Takenaka M, Fujiwara H
Department of Anesthesiology and Critical Care Medicine, Gifu University School of Medicine, Japan.
Stroke. 1998 Aug;29(8):1656-65. doi: 10.1161/01.str.29.8.1656.
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.
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) (n=6 each).
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 Nomega-nitro-L-arginine methyl ester; the initial vasoconstriction was inhibited by seratrodast, a thromboxane A2 receptor antagonist (n=6 in each case).
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+ channel activation. The vasoconstriction is partially due to thromboxane A2 induced by cigarette smoke.
急性吸烟对脑循环的影响存在争议。本研究旨在（1）阐明吸烟与输注尼古丁的作用之间以及单支烟与多支烟吸烟对脑血管的作用之间的差异，（2）探究血管反应的潜在机制。
在戊巴比妥麻醉、机械通气的Sprague-Dawley大鼠中，使用颅骨开窗标本测量软脑膜血管直径。我们研究了以下因素的作用：（1）每分钟吸60口来自两种尼古丁水平（每支烟分别含0.1毫克和1毫克）香烟的主流烟雾；（2）静脉注射尼古丁（每只动物0.05毫克）；（3）重复吸烟（每隔30分钟吸4支含1毫克尼古丁的香烟）（每组n = 6）。
吸入含0.1毫克或1毫克尼古丁香烟的烟雾1分钟，导致软脑膜小动脉在30秒时收缩（分别为7.2%和7.3%），随后扩张（在5至10分钟时达到峰值；分别为4.6%和17.9%）。输注尼古丁导致软脑膜血管扩张（35.7%），且无初始血管收缩。重复吸烟抑制了软脑膜血管扩张，但未抑制初始血管收缩。单支烟引起的血管扩张在使用美加明或格列本脲预处理后受到极大抑制，普萘洛尔或Nω-硝基-L-精氨酸甲酯使其减弱；初始血管收缩受到血栓素A2受体拮抗剂塞曲司特的抑制（每种情况n = 6）。
单支烟吸烟对脑小动脉张力有显著的双相作用。重复吸烟使血管扩张减弱。血管扩张很可能是尼古丁的作用，至少部分是通过交感神经激活、一氧化氮生成和钾通道激活介导的。血管收缩部分归因于香烟烟雾诱导的血栓素A2。
