Nariai T, Senda M, Ishii K, Wakabayashi S, Yokota T, Toyama H, Matsushima Y, Hirakawa K
Department of Neurosurgery, School of Medicine, Tokyo Medical and Dental University, and the Positron Medical Center, Japan.
Stroke. 1998 Jul;29(7):1281-92. doi: 10.1161/01.str.29.7.1281.
The alteration of regional cerebral blood flow (CBF) during and after hyperventilation was measured using positron emission tomography (PET) to determine the circulatory response induced by daily respiratory changes in the cerebral area under chronic hemodynamic stress.
Three normal volunteers and 12 patients with an obstruction of major cerebral arteries underwent PET measurements of the CBF after an injection of H2(15)O: (1) in the resting condition, (2) during hyperventilation (HV scan), (3) 1 to 3 minutes after hyperventilation (post-HV scan), (4) during the inhalation of 5% CO2, and (5) after an injection of acetazolamide. Eleven patients also underwent a 15O gas study to measure CBF, oxygen extraction fraction (OEF), and cerebral blood volume (CBV).
(1) In 9 patients, the CBF value in the post-HV scan was lower than that in the HV scan in 1 or more regions in the area of the obstructed arteries, although the PaCO2 level during the post-HV scan was higher than that during the HV scan in all patients. All control regions in the patients and in the normal volunteers showed an elevated CBF in the post-HV scan compared with the HV scan. (2) The negative post-HV response (posthyperventilatory steal) was prominent in 4 patients with moyamoya vessels and in another 5 patients with atherosclerotic disease who had PET evidence of hemodynamic stress (elevated CBV or OEF). (3) The regional pre- to post-HV change in CBF was significantly correlated with the CBF responses to acetazolamide and CO2.
Vasodilatation after the termination of hyperventilation in the normal areas induces a steal response in the cerebral area suffering from hemodynamic stress and may cause profound hypoperfusion in everyday situations. This phenomenon may be important to our understanding of the clinical symptoms and the natural course of chronic cerebral occlusive disease bearing hemodynamic stress.
使用正电子发射断层扫描（PET）测量过度换气期间及之后局部脑血流量（CBF）的变化，以确定慢性血流动力学应激下脑区每日呼吸变化所诱发的循环反应。
3名正常志愿者和12名大脑主要动脉阻塞患者在注射H2(15)O后接受PET测量CBF：（1）静息状态下；（2）过度换气期间（HV扫描）；（3）过度换气后1至3分钟（HV后扫描）；（4）吸入5% CO2期间；（5）注射乙酰唑胺后。11名患者还接受了15O气体研究以测量CBF、氧摄取分数（OEF）和脑血容量（CBV）。
（1）9名患者中，尽管所有患者HV后扫描期间的动脉血二氧化碳分压（PaCO2）水平高于HV扫描期间，但在阻塞动脉区域的1个或更多区域中，HV后扫描的CBF值低于HV扫描。患者和正常志愿者的所有对照区域在HV后扫描中与HV扫描相比CBF均升高。（2）4名烟雾病患者和另外5名有PET血流动力学应激证据（CBV或OEF升高）的动脉粥样硬化疾病患者中，HV后负反应（过度换气后盗血）明显。（3）CBF的局部HV前后变化与对乙酰唑胺和CO2的CBF反应显著相关。
正常区域过度换气终止后的血管扩张在遭受血流动力学应激的脑区诱发盗血反应，并可能在日常情况下导致严重的灌注不足。这种现象对于我们理解伴有血流动力学应激的慢性脑闭塞性疾病的临床症状和自然病程可能很重要。
