Department of Radiology, Center for Functional MRI, University of California San Diego School of Medicine , La Jolla, California.
Division of Physiology, Department of Medicine, University of California San Diego School of Medicine , La Jolla, California.
J Appl Physiol (1985). 2017 Dec 1;123(6):1477-1486. doi: 10.1152/japplphysiol.00341.2017. Epub 2017 Jul 13.
Ventilation and cerebral blood flow (CBF) are both sensitive to hypoxia and hypercapnia. To compare chemosensitivity in these two systems, we made simultaneous measurements of ventilatory and cerebrovascular responses to hypoxia and hypercapnia in 35 normal human subjects before and after acclimatization to hypoxia. Ventilation and CBF were measured during stepwise changes in isocapnic hypoxia and iso-oxic hypercapnia. We used MRI to quantify actual cerebral perfusion. Measurements were repeated after 2 days of acclimatization to hypoxia at 3,800 m altitude (partial pressure of inspired O = 90 Torr) to compare plasticity in the chemosensitivity of these two systems. Potential effects of hypoxic and hypercapnic responses on acute mountain sickness (AMS) were assessed also. The pattern of CBF and ventilatory responses to hypercapnia were almost identical. CO responses were augmented to a similar degree in both systems by concomitant acute hypoxia or acclimatization to sustained hypoxia. Conversely, the pattern of CBF and ventilatory responses to hypoxia were markedly different. Ventilation showed the well-known increase with acute hypoxia and a progressive decline in absolute value over 25 min of sustained hypoxia. With acclimatization to hypoxia for 2 days, the absolute values of ventilation and O sensitivity increased. By contrast, O sensitivity of CBF or its absolute value did not change during sustained hypoxia for up to 2 days. The results suggest a common or integrated control mechanism for CBF and ventilation by CO but different mechanisms of O sensitivity and plasticity between the systems. Ventilatory and cerebrovascular responses were the same for all subjects irrespective of AMS symptoms. NEW & NOTEWORTHY Ventilatory and cerebrovascular hypercapnic response patterns show similar plasticity in CO sensitivity following hypoxic acclimatization, suggesting an integrated control mechanism. Conversely, ventilatory and cerebrovascular hypoxic responses differ. Ventilation initially increases but adapts with prolonged hypoxia (hypoxic ventilatory decline), and ventilatory sensitivity increases following acclimatization. In contrast, cerebral blood flow hypoxic sensitivity remains constant over a range of hypoxic stimuli, with no cerebrovascular acclimatization to sustained hypoxia, suggesting different mechanisms for O sensitivity in the two systems.
通气和脑血流（CBF）对低氧和高碳酸血症均敏感。为了比较这两个系统的化学敏感性，我们在 35 名正常人体在适应低氧前后，同时测量了低氧和高碳酸血症对通气和脑血管的反应。在等碳酸缺氧和等氧高碳酸的逐步变化过程中测量了通气和 CBF。我们使用 MRI 来量化实际的脑灌注。在海拔 3800 米（吸入 O 分压 = 90 托）适应低氧 2 天后，重复了这些测量，以比较这两个系统的化学敏感性的可塑性。还评估了低氧和高碳酸反应对急性高原病（AMS）的潜在影响。CBF 和通气对高碳酸的反应模式几乎相同。在这两个系统中，急性低氧或适应持续低氧都会使 CO 反应同等程度地增强。相反，CBF 和通气对低氧的反应模式明显不同。通气在急性低氧时表现出众所周知的增加，并且在持续低氧 25 分钟内绝对值逐渐下降。在适应低氧 2 天后，通气和 O 敏感性的绝对值增加。相比之下，在长达 2 天的持续低氧期间，CBF 的 O 敏感性或其绝对值没有变化。结果表明，CO 对 CBF 和通气具有共同或综合的控制机制，但两个系统之间的 O 敏感性和可塑性机制不同。无论 AMS 症状如何，通气和脑血管对所有受试者的反应都是相同的。
新的和值得注意的是，在低氧适应后，CO 敏感性的通气和脑血管高碳酸反应模式显示出相似的可塑性，这表明存在一个综合控制机制。相反，通气和脑血管的低氧反应不同。通气最初增加，但随着缺氧时间的延长而适应（低氧性通气下降），并且适应后通气敏感性增加。相比之下，脑血流对低氧的敏感性在一系列低氧刺激下保持不变，对持续低氧没有脑血管适应，这表明两个系统中 O 敏感性的机制不同。
