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 ma y be receiving it as a premedication before surgery, the authors inves tigated its effect on cerebral hemodynamics. Methods: In nine voluntee rs, middle cerebral artery mean blood flow velocity (Vm) was measured using transcranial Doppler ultrasonography (TCD). CO2 vasoreactivity w as measured before clonidine administration (preclonidine), 00 min aft er clonidine, 5 mu g/kg orally, then following restoration of mean art erial pressure (MAP) to the preclonidine level. In addition, Vm was me asured after a phenylephrine-induced 30 mmHg increase in MAP. Results: After clonidine administration, Vm decreased from 62 +/- 9 to 48 +/- 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); rest oring MAP to the preclonidine level increased the slope to 1.60 +/- 0. 5 cm . s(-1). mmHg(-1), still less than the preclonidine slope CP < 0. 05). CO2 vasoreactivity expressed as a percentage change in Vm, decrea sed 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%/ mm Hg. With a 30-mmHg increase in MAP, Vm increased by 13% before and aft er clonidine (P < 0.05). Conclusions: Clonidine, 5 mu g/kg orally, dec reases Vm and slightly attenuates cerebral CO2 vasoreactivity, therefo re decreased cerebral blood flow and mildly attenuated CO2 vasoreactiv ity should be anticipated.