Influence of cerebrovascular function on the hypercapnic ventilatory response in healthy humans
Influence of cerebrovascular function on the hypercapnic ventilatory response in healthy humans
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DOI：
10.1113/jphysiol.2006.110627
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发表时间：
2006-11-15
影响因子：
5.5
通讯作者：
Dempsey, Jerome A.
中科院分区：
文献类型：
--
作者：
Xie, Ailiang;Skatrud, James B.;Dempsey, Jerome A.
中枢化学感受器环境中[H+]的一个重要决定因素是脑血流量。因此，我们假设脑灌注减少或脑血管对CO2的反应性降低将导致换气过度和对CO2的呼吸反应性增加。我们使用口服吲哚美辛降低脑血管对CO2的反应性，并在正常氧和高氧（50%O-2）下测试了9名正常清醒受试者对CO2的稳态高碳酸血症缓解反应。在摄入吲哚美辛后90分钟，大脑中动脉的脑血流速度（CBFV）下降至初始值的77 ± 5%，对高碳酸血症的CBFV反应的平均斜率下降至常氧对照的31（1.92 vs 0.59 cm（-1）s（-1）mmHg（-1），P < 0.05），高氧组为对照组的37%（1.58 vs 0.59 cm（-1）s（-1）mmHg（-1），P < 0.05）。与此同时，吲哚美辛给药也引起了40-60%的斜率增加，平均缓解反应CO2在两个常氧（1.27 +/- 0.31 vs 1.76 +/- 0.37 l min（-1）mmHg（-1），P < 0.05）和高氧（1.08 +/- 0.22 vs 1.79 +/- 0.37 l min（-1）mmHg（-1），P < 0.05）。这些相关的研究结果是一致的结论，脑血管对CO2的反应性是一个重要的决定因素，eupnoeic通气和高碳酸血症的呼吸反应，在人类，主要是通过其在中央化学感受器的水平的影响。
An important determinant of [H+] in the environment of the central chemoreceptors is cerebral blood flow. Accordingly we hypothesized that a reduction of brain perfusion or a reduced cerebrovascular reactivity to CO2 would lead to hyperventilation and an increased ventilatory responsiveness to CO2. We used oral indomethacin to reduce the cerebrovascular reactivity to CO2 and tested the steady-state hypercapnic ventilatory response to CO2 in nine normal awake human subjects under normoxia and hyperoxia (50% O-2). Ninety minutes after indomethacin ingestion, cerebral blood flow velocity (CBFV) in the middle cerebral artery decreased to 77 +/- 5% of the initial value and the average slope of CBFV response to hypercapnia was reduced to 31% of control in normoxia (1.92 versus 0.59 cm(-1) s(-1) mmHg(-1), P < 0.05) and 37% of control in hyperoxia (1.58 versus 0.59 cm(-1) s(-1) mmHg(-1), P < 0.05). Concomitantly, indomethacin administration also caused 40-60% increases in the slope of the mean ventilatory response to CO2 in both normoxia (1.27 +/- 0.31 versus 1.76 +/- 0.37 l min(-1) mmHg(-1), P < 0.05) and hyperoxia (1.08 +/- 0.22 versus 1.79 +/- 0.37 l min(-1) mmHg(-1), P < 0.05). These correlative findings are consistent with the conclusion that cerebrovascular responsiveness to CO2 is an important determinant of eupnoeic ventilation and of hypercapnic ventilatory responsiveness in humans, primarily via its effects at the level of the central chemoreceptors.