Carr Jay M J R, Caldwell Hannah G, Ainslie Philip N
Centre for Heart, Lung and Vascular Health, University of British Columbia - Okanagan Campus, British Columbia, Canada.
Exp Physiol. 2021 Jul;106(7):1425-1448. doi: 10.1113/EP089446. Epub 2021 May 20.
What is the topic of this review? Cerebrovascular reactivity to CO , which is a principal factor in determining ventilatory responses to CO through the role reactivity plays in determining cerebral extra- and intracellular pH. What advances does it highlight? Recent animal evidence suggests central chemoreceptor vasculature may demonstrate regionally heterogeneous cerebrovascular reactivity to CO , potentially as a protective mechanism against excessive CO washout from the central chemoreceptors, thereby allowing ventilation to reflect the systemic acid-base balance needs (respiratory changes in ) rather than solely the cerebral needs. Ventilation per se does not influence cerebrovascular reactivity independent of changes in .
Alveolar ventilation and cerebral blood flow are both predominantly regulated by arterial blood gases, especially arterial , and so are intricately entwined. In this review, the fundamental mechanisms underlying cerebrovascular reactivity and central chemoreceptor control of breathing are covered. We discuss the interaction of cerebral blood flow and its reactivity with the control of ventilation and ventilatory responsiveness to changes in , as well as the lack of influence of ventilation itself on cerebrovascular reactivity. We briefly summarize the effects of arterial hypoxaemia on the relationship between ventilatory and cerebrovascular response to both and . We then highlight key methodological considerations regarding the interaction of reactivity and ventilatory sensitivity, including the following: regional heterogeneity of cerebrovascular reactivity; a pharmacological approach for the reduction of cerebral blood flow; reactivity assessment techniques; the influence of mean arterial blood pressure; and sex-related differences. Finally, we discuss ventilatory and cerebrovascular control in the context of high altitude and congestive heart failure. Future research directions and pertinent questions of interest are highlighted throughout.
本综述的主题是什么？脑血管对二氧化碳的反应性，这是通过反应性在决定脑内和细胞内pH值中所起的作用来决定对二氧化碳通气反应的一个主要因素。它突出了哪些进展？最近的动物证据表明，中枢化学感受器血管系统对二氧化碳的脑血管反应性可能存在区域异质性，这可能是一种保护机制，可防止中枢化学感受器过度排出二氧化碳，从而使通气反映全身酸碱平衡需求（ 中的呼吸变化），而不仅仅是脑部需求。通气本身并不独立于 的变化而影响脑血管反应性。
肺泡通气和脑血流量主要都受动脉血气，尤其是动脉 的调节，因此两者紧密相连。在本综述中，涵盖了脑血管反应性和呼吸中枢化学感受器控制的基本机制。我们讨论了脑血流量及其反应性与通气控制以及对 变化的通气反应性之间的相互作用，以及通气本身对脑血管反应性缺乏影响。我们简要总结了动脉低氧血症对通气和脑血管对 和 的反应之间关系的影响。然后，我们强调了关于反应性和通气敏感性相互作用的关键方法学考虑因素，包括以下几点：脑血管反应性的区域异质性；降低脑血流量的药理学方法；反应性评估技术；平均动脉血压的影响；以及性别相关差异。最后，我们在高原和充血性心力衰竭的背景下讨论通气和脑血管控制。全文突出了未来的研究方向和相关的有趣问题。
