Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 553-558 |
| Number of pages | 6 |
| Journal | Anesthesiology |
| Volume | 87 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1997 Oct 21 |
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Keywords
- α agonist: clonidine
- Administration: oral
- Cerebral: blood flow velocity; CO vasoreactivity; autoregulation
- Monitoring, cerebral: transcranial Doppler ultrasonography, Pa(CO)
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine
Cite this
The effect of clonidine on cerebral blood flow velocity, carbon dioxide cerebral vasoreactivity, and response to increased arterial pressure in human volunteers. / Lee, Hye Won; Caldwell, James E.; Dodson, Barbara; Talke, Pekka; Howley, Joan.
In: Anesthesiology, Vol. 87, No. 3, 21.10.1997, p. 553-558.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The effect of clonidine on cerebral blood flow velocity, carbon dioxide cerebral vasoreactivity, and response to increased arterial pressure in human volunteers
AU - Lee, Hye Won
AU - Caldwell, James E.
AU - Dodson, Barbara
AU - Talke, Pekka
AU - Howley, Joan
PY - 1997/10/21
Y1 - 1997/10/21
N2 - 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.
AB - 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.
KW - α agonist: clonidine
KW - Administration: oral
KW - Cerebral: blood flow velocity; CO vasoreactivity; autoregulation
KW - Monitoring, cerebral: transcranial Doppler ultrasonography, Pa(CO)
UR - http://www.scopus.com/inward/record.url?scp=0030755068&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030755068&partnerID=8YFLogxK
U2 - 10.1097/00000542-199709000-00015
DO - 10.1097/00000542-199709000-00015
M3 - Article
C2 - 9316960
AN - SCOPUS:0030755068
VL - 87
SP - 553
EP - 558
JO - Anesthesiology
JF - Anesthesiology
SN - 0003-3022
IS - 3
ER -