The effect of clonidine on cerebral blood flow velocity, carbon dioxide cerebral vasoreactivity, and response to increased arterial pressure in human volunteers

Background: Because patients may be taking clonidine chronically or may be receiving it as a premedication before surgery, the authors investigated its effect on cerebral hemodynamics. Methods: In nine volunteers, middle cerebral artery mean blood flow velocity (Vm) was measured using transcranial Doppler ultrasonography (TCD). CO₂ vasoreactivity was measured before clonidine administration (preclonidine), 90 min after clonidine, 5 μg/kg orally, then following restoration of mean arterial pressure (MAP) to the preclonidine level. In addition, Vm was measured after a phenylephrine- induced 30-mmHg increase in MAP. Results: After clonidine administration, Vm decreased from 62 ± 9 to 48 ± 8 cm/s (P < 0.01), and MAP decreased from 86 ± 10 to 63 ± 5 mmHg (P < 0.01; mean ± SD). Clonidine decreased the CO₂ vasoreactivity slope from 2.2 ± 0.4 to 1.2 ± 0.5 cm · s^-1 · mmHg^-1 (P < 0.05); restoring MAP to the preclonidine level increased the slope to 1.60 ± 0.5 cm · s^-1 · mmHg^-1, still less than the preclonidine slope (P < 0.05). CO₂ vasoreactivity expressed as a percentage change in Vm, decreased after clonidine, 3.5 ± 0.8 versus 2.4 ± 0.8 %/mmHg (P < 0.05); this difference disappeared after restoration of MAP, 3.1 ± 1.2 %/mmHg. With a 30-mmHg increase in MAP, Vm increased by 13% before and after clonidine (P < 0.05). Conclusions: Clonidine, 5 μg/kg orally, decreases Vm and slightly attenuates cerebral CO₂ vasoreactivity, therefore decreased cerebral blood flow and mildly attenuated CO₂ vasoreactivity should be anticipated.