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人体对二氧化碳的脑血管反应。

The cerebrovascular response to carbon dioxide in humans.

机构信息

Department of Physiology, Medical Sciences Building, 1 King's College Circle, University of Toronto, Toronto, Ontario, Canada M5S 1A8.

出版信息

J Physiol. 2011 Jun 15;589(Pt 12):3039-48. doi: 10.1113/jphysiol.2011.206052. Epub 2011 Apr 26.

DOI:10.1113/jphysiol.2011.206052
PMID:21521758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3139085/
Abstract

Carbon dioxide (CO2) increases cerebral blood flow and arterial blood pressure. Cerebral blood flow increases not only due to the vasodilating effect of CO2 but also because of the increased perfusion pressure after autoregulation is exhausted. Our objective was to measure the responses of both middle cerebral artery velocity (MCAv) and mean arterial blood pressure (MAP) to CO2 in human subjects using Duffin-type isoxic rebreathing tests. Comparisons of isoxic hyperoxic with isoxic hypoxic tests enabled the effect of oxygen tension to be determined. During rebreathing the MCAv response to CO2 was sigmoidal below a discernible threshold CO2 tension, increasing from a hypocapnic minimum to a hypercapnic maximum. In most subjects this threshold corresponded with the CO2 tension at which MAP began to increase. Above this threshold both MCAv and MAP increased linearly with CO2 tension. The sigmoidal MCAv response was centred at a CO2 tension close to normal resting values (overall mean 36 mmHg). While hypoxia increased the hypercapnic maximum percentage increase in MCAv with CO2 (overall means from76.5 to 108%) it did not affect other sigmoid parameters. Hypoxia also did not alter the supra-threshold MCAv and MAP responses to CO2 (overall mean slopes 5.5% mmHg⁻¹ and 2.1 mmHg mmHg⁻¹, respectively), but did reduce the threshold (overall means from 51.5 to 46.8 mmHg). We concluded that in the MCAv response range below the threshold for the increase of MAP with CO2, the MCAv measurement reflects vascular reactivity to CO2 alone at a constant MAP.

摘要

二氧化碳(CO2)增加脑血流和动脉血压。脑血流增加不仅是由于 CO2 的血管扩张作用,还因为自动调节耗尽后灌注压增加。我们的目的是使用 Duffin 型等氧再呼吸测试测量人类受试者中大脑中动脉速度(MCAv)和平均动脉血压(MAP)对 CO2 的反应。等氧高氧与等氧低氧测试的比较使能够确定氧气张力的影响。在再呼吸期间,CO2 对 MCAv 的反应在可识别的 CO2 张力阈值以下呈 S 形,从低碳酸最小值增加到高碳酸最大值。在大多数受试者中,该阈值对应于 MAP 开始增加的 CO2 张力。在该阈值以上,MCAv 和 MAP 随 CO2 张力线性增加。S 形 MCAv 反应的中心位于接近正常静息值的 CO2 张力(总体平均值为 36mmHg)。虽然缺氧增加了 CO2 对 MCAv 的高碳酸最大百分比增加(从 76.5%到 108%的总体平均值),但它不影响其他 S 形参数。缺氧也不改变 CO2 对超阈值 MCAv 和 MAP 的反应(总体平均斜率分别为 5.5%mmHg⁻¹和 2.1mmHgmmHg⁻¹),但降低了阈值(总体平均值从 51.5mmHg 降至 46.8mmHg)。我们得出结论,在 MCAv 反应范围低于 CO2 增加 MAP 的阈值,MCAv 测量仅反映在恒定 MAP 下 CO2 的血管反应性。

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Influence of changes in blood pressure on cerebral perfusion and oxygenation.血压变化对脑灌注和氧合的影响。
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