Abstract
The influence of sympathetic nervous activity on the cerebral circulation and cerebrovascular CO2 reactivity were investigated through the inhibition of dopamine-beta-hydroxylase (DBH), the final enzyme in the biosynthesis of norepinephrine.
1) Intravenous infusion of fusaric acid (a potent DBH inhibitor) increased cerebrocortical PO2 and CBF shortly after the administration, with no significant changes in cerebrocortical PCO2. The mean arterial blood pressure decreased in a few minutes after infusion of fusaric acid.
2) The increase in cerebrocortical PO2 and CBF during 5% CO2 inhalation was significantly augmented after DBH inhibition with fusaric acid. There were no significant differences in the changes of arterial blood gases and pH during CO2 inhalation before and after DBH inhibition. The increase of arterial blood pressure during CO2 inhalation was reduced after DBH inhibition.
3) The decrease in the cerebrocortical PO2 and CBF during hyperventilation was slightly attenuated after DBH inhibition, which was not statisticaly significant.
The cerebral vasodilatation caused by fusaric acid and augmented cerebrovascular CO2 reactivity after DBH inhibition suggest that the sympathetic nervous system influences cerebral vascular tone and plays a role in modulating chemical vasomotor activity.
