Terborg Christoph, Bramer Silke, Weiller Cornelius, Röther Joachim
Department of Neurology, Friedrich-Schiller University of Jena, Philosophenweg 3, 07740 Jena, Germany.
J Neurol Sci. 2002 Dec 15;205(1):15-20. doi: 10.1016/s0022-510x(02)00308-8.
Cigarette smoking is a major risk factor for stroke, and quitting reduces the stroke risk within a few years. The aim of our study was to clarify whether CO(2)-induced vasomotor reactivity (VMR) is impaired in smokers after smoking a cigarette as a possible factor of an increased stroke risk. We compared VMR of 23 healthy smokers assessed at baseline, immediately, and 30 min after smoking a cigarette (1.2 mg nicotine) with values from nonsmoking, age-matched controls (n=24), obtained at identical time intervals. Cerebral blood flow velocities (CBFV) of both middle cerebral arteries (transcranial Doppler sonography), changes in concentration of cerebral oxygenated, deoxygenated, and total hemoglobin (HbO(2), Hb, and HbT, near-infrared spectroscopy), mean arterial blood pressure (MAP), and skin blood flow were recorded during normo- and hypercapnia. VMR was calculated as percentage change in CBFV and as micromolar change in concentration of HbO(2), Hb, and HbT per 1% increase in endtidal CO(2). CBFV in smokers was increased at baseline (left, p<0.05; right, p=0.05), immediately (p<0.01), and 30 min after smoking (p<0.05) as compared with nonsmokers. MAP rose immediately after smoking (p<0.01) and declined after 30 min. VMR in smokers at baseline did not differ from controls, decreased immediately after smoking (p<0.05), and normalized after 30 min (p>0.05). Increased baseline CBFV in smokers after smoking might be due to arteriolar dilation, increased MAP, and possibly constriction of basal cerebral arteries. Impaired VMR for about 30 min after smoking reflects endothelial dysfunction. This might contribute to the enhanced stroke risk in smokers.
吸烟是中风的主要风险因素，戒烟可在数年内降低中风风险。我们研究的目的是阐明吸烟后吸烟者的二氧化碳诱导血管舒缩反应性（VMR）是否受损，这可能是中风风险增加的一个因素。我们将23名健康吸烟者在基线、吸烟（1.2毫克尼古丁）后即刻和30分钟时的VMR与年龄匹配的非吸烟对照组（n = 24）在相同时间间隔测得的值进行了比较。在正常和高碳酸血症期间记录双侧大脑中动脉的脑血流速度（经颅多普勒超声）、脑氧合血红蛋白、脱氧血红蛋白和总血红蛋白浓度（HbO₂、Hb和HbT，近红外光谱）、平均动脉血压（MAP）以及皮肤血流的变化。VMR计算为脑血流速度的百分比变化以及每呼气末二氧化碳增加1%时HbO₂、Hb和HbT浓度的微摩尔变化。与非吸烟者相比，吸烟者的脑血流速度在基线时升高（左侧，p < 0.05；右侧，p = 0.05），吸烟后即刻升高（p < 0.01），30分钟后仍升高（p < 0.05）。MAP在吸烟后即刻升高（p < 0.01），30分钟后下降。吸烟者基线时的VMR与对照组无差异，吸烟后即刻降低（p < 0.05），30分钟后恢复正常（p > 0.05）。吸烟后吸烟者基线脑血流速度增加可能是由于小动脉扩张、MAP升高以及可能的基底脑动脉收缩。吸烟后约30分钟VMR受损反映了内皮功能障碍。这可能导致吸烟者中风风险增加。
