Terborg Christoph, Birkner Thomas, Schack Bärbel, Witte Otto W
Department of Neurology, Friedrich-Schiller University of Jena, Philosophenweg 3, 07740 Jena, Germany.
J Neurol Sci. 2002 Dec 15;205(1):71-5. doi: 10.1016/s0022-510x(02)00311-8.
Cigarette smoking has been shown to increase cerebral blood flow velocity (CBFV) and reduce vasomotor reactivity temporarily. The aim of our study was to clarify whether this results from dilation of resistance vessels alone with subsequent increase in regional cerebral blood flow (rCBF), or an additional constriction of basal cerebral arteries. In 24 healthy smokers (mean age+/-S.D., 32.7+/-10.5 years), cerebral oxygenation and hemodynamics were monitored by transcranial Doppler sonography and near-infrared spectroscopy before, during, and after smoking a cigarette (nicotine 0.9 mg). We simultaneously recorded CBFV of both middle cerebral arteries, mean arterial blood pressure, skin blood flow, end-tidal CO(2), changes in concentration of cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin (micromol/l), and a cerebral tissue oxygenation index. Smoking increased CBFV (p<0.01), oxyhemoglobin (p<0.01), and total hemoglobin (p<0.01). After smoking, the increase in CBFV and total hemoglobin persisted (p<0.01), while oxyhemoglobin returned to baseline. Deoxyhemoglobin and cerebral tissue oxygenation index did not change during the whole procedure. During, but not after smoking, CBFV increase was correlated to ipsilateral changes in oxyhemoglobin and total hemoglobin (p<0.05). The increase in oxyhemoglobin only during smoking and the lack of changes in deoxyhemoglobin and cerebral tissue oxygenation index indicate that smoking did not substantially increase rCBF. The smoking-induced elevation in CBFV might therefore be due to an additional constriction of the middle cerebral artery. The combined effects of smoking on basal cerebral arteries and arterioles might contribute to the increased stroke risk in smokers.
研究表明，吸烟会使脑血流速度（CBFV）增加，并暂时降低血管运动反应性。我们研究的目的是明确这是否仅由阻力血管扩张导致局部脑血流量（rCBF）随后增加引起，还是脑基底动脉也会额外收缩。在24名健康吸烟者（平均年龄±标准差，32.7±10.5岁）中，于吸一支香烟（尼古丁0.9毫克）之前、期间和之后，通过经颅多普勒超声和近红外光谱法监测脑氧合和血流动力学。我们同时记录了双侧大脑中动脉的CBFV、平均动脉血压、皮肤血流量、呼气末二氧化碳、脑氧合血红蛋白、脱氧血红蛋白和总血红蛋白浓度变化（微摩尔/升）以及脑组织氧合指数。吸烟使CBFV（p<0.01）、氧合血红蛋白（p<0.01）和总血红蛋白（p<0.01）增加。吸烟后，CBFV和总血红蛋白的增加持续存在（p<0.01），而氧合血红蛋白恢复至基线水平。在整个过程中，脱氧血红蛋白和脑组织氧合指数未发生变化。在吸烟期间而非吸烟后，CBFV的增加与同侧氧合血红蛋白和总血红蛋白的变化相关（p<0.05）。仅在吸烟期间氧合血红蛋白增加，以及脱氧血红蛋白和脑组织氧合指数缺乏变化，表明吸烟并未使rCBF显著增加。因此，吸烟引起的CBFV升高可能是由于大脑中动脉额外收缩所致。吸烟对脑基底动脉和小动脉的综合作用可能导致吸烟者中风风险增加。
