Ellingsen I, Hauge A, Nicolaysen G, Thoresen M, Walløe L
Acta Physiol Scand. 1987 Feb;129(2):157-63. doi: 10.1111/j.1748-1716.1987.tb08054.x.
The effect of moderate hypoxia on cerebral blood flow (CBF) in man has not been well described, and little is known about the interaction of changes in arterial PO2 and PCO2 as regards CBF. Using a non-invasive doppler ultrasound method we have measured the instantaneous mean blood velocity (which is proportional to CBF as long as the cross-section of the vessel is constant) in the carotid artery in four healthy unanaesthetized subjects. We found in all subjects that a reduction in alveolar PO2 from about 13 to about 8.7 kPa with maintained constant alveolar PCO2 (PA, CO2) caused CBF to increase gradually over 10 min (half-time about 4 min) to about 125% of control. The CBF decreased quickly (half-time about 45 s) towards control when alveolar PO2 was reset to 13 kPa. As measured 5 min after a step-change in PA, O2, the change in CBF was independent of PA, CO2 within the range 3.3-6.7 kPa. An increase in PA, O2 to about 33 kPa reduced CBF only if PA, CO2 was in the hypercapnic range. Unexpectedly we found that the CBF response showed 'adaptation' during both maintained increase and decrease in PA, CO2. The CBF started to return towards control level within 10 min after induction of hypo- or hypercapnia. We conclude that also moderate hypoxia causes increased CBF in unanaesthetized man within a wide range of PA, CO2.
中度缺氧对人体脑血流量（CBF）的影响尚未得到充分描述，关于动脉血氧分压（PO2）和二氧化碳分压（PCO2）变化对CBF的相互作用也知之甚少。我们使用一种非侵入性多普勒超声方法，测量了4名未麻醉的健康受试者颈动脉中的瞬时平均血流速度（只要血管横截面积恒定，该速度就与CBF成正比）。我们发现，在所有受试者中，肺泡PO2从约13 kPa降至约8.7 kPa，同时肺泡PCO2（PA,CO2）保持恒定，导致CBF在10分钟内逐渐增加（半衰期约4分钟），达到对照值的约125%。当肺泡PO2恢复到13 kPa时，CBF迅速下降（半衰期约45秒）至对照值。在PA,O2发生阶跃变化5分钟后测量发现，在3.3 - 6.7 kPa范围内，CBF的变化与PA,CO2无关。只有当PA,CO2处于高碳酸血症范围时，PA,O2升高至约33 kPa才会使CBF降低。出乎意料的是，我们发现，在PA,CO2持续升高和降低的过程中，CBF反应均表现出“适应性”。在低碳酸血症或高碳酸血症诱导后10分钟内，CBF开始向对照水平恢复。我们得出结论，在广泛的PA,CO2范围内，中度缺氧也会导致未麻醉人体的CBF增加。
