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

Hye Won Lee, James E. Caldwell, Barbara Dodson, Pekka Talke, Joan Howley

Research output: Contribution to journalArticle

27 Citations (Scopus)

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 languageEnglish
Pages (from-to)553-558
Number of pages6
JournalAnesthesiology
Volume87
Issue number3
DOIs
Publication statusPublished - 1997 Oct 21

Fingerprint

Cerebrovascular Circulation
Blood Flow Velocity
Clonidine
Carbon Dioxide
Volunteers
Arterial Pressure
Doppler Transcranial Ultrasonography
Premedication
Middle Cerebral Artery
Phenylephrine
Hemodynamics

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 journalArticle

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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.",
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AU - Talke, Pekka

AU - Howley, Joan

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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.

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