Abstract
Neurovascular coupling describes a series of processes that serve to match blood supply to neuronal metabolism within the central nervous system. We know that the sympathetic nervous system plays a role in several cerebrovascular control pathways, and preclinical non‐human work demonstrates that the sympathetic nervous system may play a role in neurovascular coupling. These preclinical models utilize isolated cell preparations lacking key inputs to the neurovascular unit such as that of the autonomic nervous system, or utilize anesthetics which blunt cerebrovascular regulatory pathways.Here, our objective was to provide preliminary insight into the role of sympathetic nervous system activation in neurovascular coupling by using our non‐anesthetized, non‐stressed, human, truly in vivo model. We utilized moderate lower body negative pressure (−40 mmHg) to elevate sympathetic activity without affecting mean arterial pressure. Beat‐by‐beat blood pressure was recorded via finger photoplethysmography, while cerebral blood velocity in the middle and posterior cerebral arteries was measured via transcranial Doppler. Neurovascular coupling was elicited using our standardized visual stimulus protocol and data was analyzed using our custom software. As lower body negative pressure leads to sympatho‐excitation and hyperventilation, in a subset of individuals we maintained end‐tidal carbon dioxide levels identical to baseline during lower body negative pressure.Absolute cerebral blood velocity was influenced by arterial carbon dioxide levels. Neurovascular coupling was preserved during lower body negative pressure induced sympatho‐excitation and reduced arterial carbon dioxide levels.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada, Libin Cardiovascular Institute, Hotchkiss Brain Institute, Compute Canada
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