Institute of Cardiovascular & Metabolic Disease, University of North Texas Health Science Center , Fort Worth, Texas.
Department of Physical Therapy, University of North Texas Health Science Center , Fort Worth, Texas.
J Appl Physiol (1985). 2017 Dec 1;123(6):1689-1697. doi: 10.1152/japplphysiol.00647.2017. Epub 2017 Oct 26.
Cerebral vasodilation and increased cerebral oxygen extraction help maintain cerebral oxygen uptake in the face of hypoxemia. This study examined cerebrovascular responses to intermittent hypoxemia in eight healthy men breathing 10% O for 5 cycles, each 6 min, interspersed with 4 min of room air breathing. Hypoxia exposures raised heart rate ( P < 0.01) without altering arterial pressure, and increased ventilation ( P < 0.01) by expanding tidal volume. Arterial oxygen saturation ([Formula: see text]) and cerebral tissue oxygenation ([Formula: see text]) fell ( P < 0.01) less appreciably in the first bout (from 97.0 ± 0.3% and 72.8 ± 1.6% to 75.5 ± 0.9% and 54.5 ± 0.9%, respectively) than the fifth bout (from 94.9 ± 0.4% and 70.8 ± 1.0% to 66.7 ± 2.3% and 49.2 ± 1.5%, respectively). Flow velocity in the middle cerebral artery ( V) and cerebrovascular conductance increased in a sigmoid fashion with decreases in [Formula: see text] and [Formula: see text]. These stimulus-response curves shifted leftward and upward from the first to the fifth hypoxia bouts; thus, the centering points fell from 79.2 ± 1.4 to 74.6 ± 1.1% ( P = 0.01) and from 59.8 ± 1.0 to 56.6 ± 0.3% ( P = 0.002), and the minimum V increased from 54.0 ± 0.5 to 57.2 ± 0.5 cm/s ( P = 0.0001) and from 53.9 ± 0.5 to 57.1 ± 0.3 cm/s ( P = 0.0001) for the [Formula: see text]- V and [Formula: see text]- V curves, respectively. Cerebral oxygen extraction increased from prehypoxia 0.22 ± 0.01 to 0.25 ± 0.02 in minute 6 of the first hypoxia bout, and remained elevated between 0.25 ± 0.01 and 0.27 ± 0.01 throughout the fifth hypoxia bout. These results demonstrate that cerebral vasodilation combined with enhanced cerebral oxygen extraction fully compensated for decreased oxygen content during acute, cyclic hypoxemia. NEW & NOTEWORTHY Five bouts of 6-min intermittent hypoxia (IH) exposures to 10% O progressively reduce arterial oxygen saturation ([Formula: see text]) to 67% without causing discomfort or distress. Cerebrovascular responses to hypoxemia are dynamically reset over the course of a single IH session, such that threshold and saturation for cerebral vasodilations occurred at lower [Formula: see text] and cerebral tissue oxygenation ([Formula: see text]) during the fifth vs. first hypoxia bouts. Cerebral oxygen extraction is augmented during acute hypoxemia, which compensates for decreased arterial O content.
脑血管扩张和增加脑氧摄取有助于在低氧血症的情况下维持脑氧摄取。本研究在 8 名健康男性中检查了间歇性低氧血症对脑血管的反应，他们在 5 个周期内呼吸 10% 的 O2，每个周期 6 分钟，期间穿插 4 分钟的室内空气呼吸。低氧暴露使心率升高（P < 0.01），而不改变动脉压，并通过增加潮气量来增加通气量（P < 0.01）。动脉血氧饱和度（[Formula: see text]）和脑组织氧合（[Formula: see text]）在第一回合（从 97.0 ± 0.3%和 72.8 ± 1.6%降至 75.5 ± 0.9%和 54.5 ± 0.9%）下降幅度明显小于第五回合（从 94.9 ± 0.4%和 70.8 ± 1.0%降至 66.7 ± 2.3%和 49.2 ± 1.5%）。大脑中动脉的血流速度（V）和脑血管的传导性呈S型增加，与[Formula: see text]和[Formula: see text]的下降有关。这些刺激-反应曲线从第一到第五次低氧回合向左上方移动；因此，中心点从 79.2 ± 1.4%降至 74.6 ± 1.1%（P = 0.01）和从 59.8 ± 1.0%降至 56.6 ± 0.3%（P = 0.002），最小 V 从 54.0 ± 0.5 cm/s增加到 57.2 ± 0.5 cm/s（P = 0.0001）和从 53.9 ± 0.5 cm/s增加到 57.1 ± 0.3 cm/s（P = 0.0001）对于[Formula: see text]-V 和[Formula: see text]-V 曲线，分别。在第一次低氧回合的第 6 分钟，脑氧摄取从预低氧时的 0.22 ± 0.01增加到 0.25 ± 0.02，并且在第五次低氧回合期间一直保持在 0.25 ± 0.01 和 0.27 ± 0.01 之间。这些结果表明，在急性、周期性低氧血症期间，脑血管扩张和增强的脑氧摄取完全补偿了氧含量的降低。新的和值得注意的是，五次 6 分钟的间歇性低氧（IH）暴露到 10% 的 O2 将动脉血氧饱和度（[Formula: see text]）逐渐降低到 67%，而不会引起不适或痛苦。低氧血症对脑血管的反应在单次 IH 过程中动态重置，使得第五次低氧发作时的阈值和饱和度在较低的[Formula: see text]和脑组织氧合（[Formula: see text]）下发生。急性低氧血症时，脑氧摄取增加，补偿了动脉氧含量的降低。
