Dynamics of the cerebral blood flow response to step changes in end-tidal P-CO2 and P-O2 in humans
Dynamics of the cerebral blood flow response to step changes in end-tidal P-CO2 and P-O2 in humans
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DOI：
10.1152/jappl.1996.81.3.1084
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发表时间：
1996-09-01
影响因子：
3.3
通讯作者：
Robbins, PA
中科院分区：
文献类型：
--
作者：
Poulin, MJ;Liang, PJ;Robbins, PA
本研究检测了人类脑血流对缺氧和高碳酸血症的反应动力学。采用经颅多普勒超声连续评估大脑中动脉血流（MCAF）。MCAF在逐拍基础上计算为强度加权平均速度和反射信号的总功率的乘积。利用动态潮气末强迫系统控制潮气末PCO 2（PET（CO2））和PO 2（PET（O2））。对6名受试者重复施用4种方案中的每种方案6次。第一种是对照方案，PET（O2）始终保持在100 Torr，PET（CO2）始终保持在正常二氧化碳以上1-2 Torr。第二种是低氧步骤方案，PE（O2）从对照值降低到50 Torr，持续20 min。第三种是高碳酸血症步骤方案，PET（CO2）从对照值升高7.5 Torr，持续20 min。第四种是低氧和高碳酸血症步骤方案，持续20 min。多普勒信号的总功率保持相对恒定，表明血管的横截面积变化很小。在MCAF的初始瞬态后，在刺激的发作，没有适应或渐进式增加，观察到在剩余的20分钟。一个简单的模型组成的一个单一的纯延迟，增益项，时间常数，和偏移的开和关瞬态适合缺氧和高碳酸血症的协议。对于高碳酸血症，发作的所有参数与刺激的缓解显著不同。这种不对称的特征是开瞬态比关瞬态慢，以及高碳酸血症缓解后一定程度的下冲。最后，这项研究的结果表明，人类对缺氧和高碳酸血症的脑血流反应比以前认为的要快得多。
This study examined the dynamics of the cerebral blood flow response to hypoxia and hypercapnia in humans. Middle cerebral artery blood flow (MCAF) was assessed continuously using transcranial Doppler ultrasound. MCAF was calculated an a beat-by-beat basis as the product of the intensity-weighted mean velocity and the total power of the reflected signal. End-tidal PCO2 (PET(CO2)) and PO2 (PET(O2)) were controlled using a dynamic end-tidal forcing system. Six repeats of each of four protocols were administered to six subjects. The first was a control protocol with PET(O2) held at 100 Torr and PET(CO2) held 1-2 Torr above eucapnia throughout. The second was a hypoxic step protocol with PE(O2) lowered from control values to 50 Torr for 20 min, The third was a hypercapnic step protocol with PET(CO2) elevated from control by 7.5 Torr for 20 min. The fourth was a hypoxic-and-hypercapnic step protocol lasting 20 min. The total power of the Doppler signal remained relatively constant, suggesting that the cross-sectional area of the vessel changed little. After the initial transient in MCAF at the onset of the stimulus, no adaptation or progressive increase was observed over the remaining 20 min. A simple model consisting of a single pure delay, gain terms, time constants, and offsets for the on and off transients was fitted to the hypoxic and hypercapnic protocols. For hypercapnia, all the parameters for the onset were significantly different from the relief of the stimulus. The asymmetry was characterized by a slower on transient than off transient and also by a degree of undershoot after the relief of hypercapnia. Finally, the results from this study show that the cerebral blood flow response to hypoxia and hypercapnia in humans is much faster than has previously been thought.