Does hypercapnia-induced impairment of cerebral autoregulation affect neurovascular coupling? A functional TCD study

Author:

Maggio Paola1,Salinet Angela S. M.2,Panerai Ronney B.23,Robinson Thompson G.23

Affiliation:

1. Neurologia Clinica, Università Campus Bio-Medico, Rome, Italy;

2. Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom; and

3. National Institutes for Health Research (NIHR), Biomedical Research Unit in Cardiovascular Sciences, Clinical Sciences Wing, Glenfield Hospital, Leicester, United Kingdom

Abstract

Neurovascular coupling (NVC) and dynamic cerebral autoregulation (dCA) are both impaired in the acute phase of ischemic stroke, but their reciprocal interactions are difficult to predict. To clarify these aspects, the present study explored NVC in a healthy volunteer population during a surrogate state of impaired dCA induced by hypercapnia. This study aimed to test whether hypercapnia leads to a depression of NVC through an impairment of dCA. Continuous recordings of middle cerebral arteries cerebral blood flow velocity (CBFv), blood pressure (BP), heart rate, and end-tidal CO2 were performed in 19 right-handed subjects (aged >45 yr) before, during, and after 60 s of a passive paradigm during normocapnia and hypercapnia. The CBFv response was broken down into subcomponents describing the relative contributions of BP (VBP), critical closing pressure (VCrCP), and resistance area product (VRAP). VRAP reflects myogenic activity in response to BP changes, whereas VCrCP is more indicative of metabolic control. The results revealed that hypercapnia significantly affected NVC, with significant reductions in the relative contribution of VCrCP to the paradigm-induced increase in CBFv. The present study suggests that hypercapnia impairs both dCA and NVC, probably acting through an impairment of the metabolic component of CBF control.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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