Abstract

What is the topic of this review? Cerebrovascular reactivity to CO2 , which is a principal factor in determining ventilatory responses to CO2 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 CO2 , potentially as a protective mechanism against excessive CO2 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.

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