Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia

Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia
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DOI:
10.1152/japplphysiol.00778.2007
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发表时间:
2008-02-01
影响因子:
3.3
通讯作者:
Burgess, Keith R.
Burgess, Keith R.
中科院分区:
医学2区
文献类型:
--
作者:
Ainslie, Philip N.;Ogoh, Shigehiko;Burgess, Keith R.

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我们假设:1)在海平面急性重度缺氧,而不是高氧,会损害动态脑自动调节(CA); 2)在高海拔(HA)CA的损害将部分恢复与高氧; 3)在HA高氧,将有更大的影响血压(BP)和大脑中动脉血流速度(MCAv)的影响较小。在健康志愿者中,在常氧和急性缺氧(吸入O2分数分别为0.12和0.10; n = 10)或高氧(吸入O2分数,1.0; n = 12)时连续测量BP和MCAv。使用传递函数增益、相位和平均BP与MCAv之间的相关性评估动态CA。还获得了动脉血气。在匹配的志愿者中,在低海拔(LA; 1,400 m)和到达HA后1-2天(类似于5,400 m,n = 10)的空气呼吸和高氧期间测量相同的变量。在急性缺氧和高氧时,血压没有变化,而在HA高氧时血压下降(-11 +/-4%; P < 0.05 vs. LA)。在急性缺氧和HA时,MCAv不变;然而,急性高氧导致MCAv下降的程度大于HA(分别为-12 +/-3 vs. -5 +/-4%; P < 0.05)。而CA是不变的高氧,在低频范围内的增益减少在急性缺氧,表明CA的改善。相比之下,HA与极低频和低频范围内的传递功能增益升高相关,表明CA受损;高氧可使这些升高降低约50%(P < 0.05)。结果表明,HA高氧可部分改善CA和降低BP,对MCAv影响不大。
We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O-2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1-2 days after arrival at HA (similar to 5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (-11 +/- 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (-12 +/- 3 vs. -5 +/- 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low- frequency range, indicating CA impairment; hyperoxia lowered these elevations by similar to 50% (P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.