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持续低氧期间脑血流量对通气抑制无影响。

No effect of brain blood flow on ventilatory depression during sustained hypoxia.

作者信息

Suzuki A, Nishimura M, Yamamoto H, Miyamoto K, Kishi F, Kawakami Y

机构信息

First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.

出版信息

J Appl Physiol (1985). 1989 Apr;66(4):1674-8. doi: 10.1152/jappl.1989.66.4.1674.

Abstract

Minute ventilation (VE) during sustained hypoxia is not constant but begins to decline within 10-25 min in adult humans. The decrease in brain tissue PCO2 may be related to this decline in VE, because hypoxia causes an increase in brain blood flow, thus resulting in enhanced clearance of CO2 from the brain tissue. To examine the validity of this hypothesis, we measured VE and arterial and internal jugular venous blood gases simultaneously and repeatedly in 15 healthy male volunteers during progressive and subsequent sustained isocapnic hypoxia (arterial PO2 = 45 Torr) for 20 min. It was assumed that jugular venous PCO2 was an index of brain tissue PCO2. Mean VE declined significantly from the initial (16.5 l/min) to the final phase (14.1 l/min) of sustained hypoxia (P less than 0.05). Compared with the control (50.9 Torr), jugular venous PCO2 significantly decreased to 47.4 Torr at the initial phase of hypoxia but did not differ among the phases of hypoxia (47.2 Torr for the intermediate phase and 47.7 Torr for the final phase). We classified the subjects into two groups by hypoxic ventilatory response during progressive hypoxia at the mean value. The decrease in VE during sustained hypoxia was significant in the low responders (n = 9) [13.2 (initial phase) to 9.3 l/min (final phase of hypoxia), P less than 0.01], but not in the high responders (n = 6) (20.9-21.3 l/min, NS). This finding could not be explained by the change of arterial or jugular venous gases, which did not significantly change during sustained hypoxia in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在成年人中,持续低氧期间的分钟通气量(VE)并非恒定不变,而是在10 - 25分钟内开始下降。脑组织PCO2的降低可能与VE的这种下降有关,因为低氧会导致脑血流量增加,从而使脑组织中CO2的清除增强。为了检验这一假设的正确性,我们在15名健康男性志愿者进行渐进性及随后持续的等碳酸血症性低氧(动脉血氧分压 = 45托)20分钟期间,同时反复测量了VE以及动脉血和颈内静脉血的气体成分。假设颈静脉PCO2是脑组织PCO2的指标。持续低氧从初始阶段(16.5升/分钟)到最后阶段(14.1升/分钟)时,平均VE显著下降(P小于0.05)。与对照组(50.9托)相比,低氧初始阶段颈静脉PCO2显著降至47.4托,但在低氧各阶段之间无差异(中间阶段为47.2托,最后阶段为47.7托)。我们根据渐进性低氧期间的低氧通气反应平均值将受试者分为两组。在低反应者(n = 9)中,持续低氧期间VE的下降显著[从13.2(初始阶段)降至9.3升/分钟(低氧最后阶段),P小于0.01],而在高反应者(n = 6)中则不显著(20.9 - 21.3升/分钟,无显著性差异)。这一发现无法用动脉血或颈静脉血气体成分的变化来解释,因为在持续低氧期间两组的这些指标均无显著变化。(摘要截断于250字)

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