Jensen J B, Sperling B, Severinghaus J W, Lassen N A
Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
J Appl Physiol (1985). 1996 Apr;80(4):1214-8. doi: 10.1152/jappl.1996.80.4.1214.
The fractional increase in cerebral blood flow (CBF) velocity (VCBF) from the control value with 5-min steps of isocapnic hypoxia and hyperoxic hypercapnia was measured by transcranial Doppler in six sea-level native men before and during a 5-day sojourn at 3,810 m altitude to determine whether cerebral vasoreactivity to low arterial O2 saturation (SaO2) gradually increased [as does the hypoxic ventilatory response (HVR)] or diminished (adapted, in concert with known slow fall of CBF) at altitude. A control resting PCO2 value was chosen each day during preliminary hyperoxia to set ventilation at 140 ml.kg-1.min-1 for this and the parallel HVR study, attempting to establish control cerebrospinal fluid (CSF) and brain extracellular fluid pH values unaltered by acclimatization. The relationship of CBF to SaO2 was nonlinear, steepening at a lower SaO2. A hyperbolic equation was used to describe hypoxic cerebrovascular reactivity: fractional VCBF = x[60/ (SaO2-40)-1], where X is the fractional increase of VCBF at 70%.X rose from 0.346 +/- 0.104 (SD) at sea level to 0.463 +/- 0.084 on altitude day 5 (P < 0.05 by paired t-test, justified by the a priori experimental plan). For comparison with CO2 sensitivity, from these X values, we estimate the rise in CBF in response to a 1% fall in SaO2 at 80% to be 1.30% at sea level and 1.74% after 5 days at altitude. CBF sensitivity to increased end-tidal PCO2 rose from 4.01 +/- 0.62%/Torr at sea level to 5.12 +/- 0.79%/Torr on day 5 (P < 0.05), as expected, at the lower PCO2 due to the logarithmic relationship of PCO2 to CSF pH. This change was not significant after correction to log PCO2. We conclude that the cerebral vascular response to acute isocapnic hypoxia may increase during acclimatization at high altitude. The mechanism is unknown but is presumably unrelated to the parallel carotid chemosensitization that, in these subjects, increased the HVR by 60% in the same 5-day period from 0.91 +/- 0.38 to 1.46 +/- 0.59 l.min-1.% fall in SaO2-1).
在6名海平面出生的男性于海拔3810米处停留5天的前后，通过经颅多普勒测量了在等容性低氧和高氧性高碳酸血症情况下，脑血流（CBF）速度（VCBF）相对于对照值以5分钟为步长的分数增加情况，以确定脑对低动脉血氧饱和度（SaO2）的血管反应性是逐渐增加（如同低氧通气反应（HVR）那样）还是降低（适应，与已知的CBF缓慢下降一致）。在初步高氧期间，每天选择一个对照静息PCO2值，将通气设定为140 ml·kg-1·min-1，用于本研究及平行的HVR研究，试图建立不受适应影响的对照脑脊液（CSF）和脑细胞外液pH值。CBF与SaO2的关系是非线性的，在较低的SaO2时变陡。使用双曲线方程来描述低氧性脑血管反应性：分数VCBF = x[60 / (SaO2 - 40) - 1]，其中X是70%时VCBF的分数增加。X从海平面时的0.346 ± 0.104（标准差）升至海拔第5天时的0.463 ± 0.084（配对t检验，P < 0.05，根据先验实验计划合理）。为了与CO2敏感性进行比较，从这些X值我们估计，在80%时SaO2每下降1%，CBF在海平面时升高1.30%，在海拔5天后升高1.74%。CBF对呼气末PCO2升高的敏感性从海平面时的4.01 ± 0.62%/Torr升至第5天时的5.12 ± 0.79%/Torr（P < 0.05），正如预期的那样，由于PCO2与CSF pH的对数关系，在较低的PCO2时出现这种情况。校正到对数PCO2后，这种变化不显著。我们得出结论，在高海拔适应过程中，脑对急性等容性低氧的血管反应可能会增加。其机制尚不清楚，但推测与平行的颈动脉化学感受性增强无关，在这些受试者中，在相同的5天时间里，颈动脉化学感受性使HVR从0.91 ± 0.38升至1.46 ± 0.59 l·min-1·% SaO2下降-1，增加了60%。
