Modification of cerebrovascular CO2 reactivity by inhibition of dopamine beta-hydroxylase.

The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated through inhibition of dopamine beta-hydroxylase (DBH). A PO2 electrode, a PCO2 electrode and a plate-type thermocouple-flowmeter were placed on the pial surface of the cat brain. Cerebrocortical PO2, PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 10 mg/kg of fusaric acid, a potent DBH inhibitor. The effects of 5% CO2 inhalation and hyperventilation were measured before and after the inhibition of DBH. Following the intracarotid infusion of fusaric acid, cerebrocortical PO2 and cerebrocortical blood flow increased significantly. After the inhibition of DBH, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was enhanced while the degree of the decrease in cerebrocortical PO2 during hyperventilation did not show any significant change. The cerebral vasodilatation caused by fusaric acid suggests that the sympathetic nervous system takes part in the resting tone of cerebral blood vessels. The increase in the cerebrovascular CO2 reactivity produced by the inhibition of DBH suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.