Effects of clonidine on human middle cerebral artery flow velocity and cerebrovascular CO2 response during sevoflurane anesthesia

Citation
T. Maekawa et al., Effects of clonidine on human middle cerebral artery flow velocity and cerebrovascular CO2 response during sevoflurane anesthesia, J NEUROS AN, 11(3), 1999, pp. 173-177
Citations number
27
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
JOURNAL OF NEUROSURGICAL ANESTHESIOLOGY
ISSN journal
08984921 → ACNP
Volume
11
Issue
3
Year of publication
1999
Pages
173 - 177
Database
ISI
SICI code
0898-4921(199907)11:3<173:EOCOHM>2.0.ZU;2-H
Abstract
The present study was designed to evaluate the effects of clonidine on huma n middle cerebral artery flow velocity and the cerebrovascular CO2 response during sevoflurane anesthesia using transcranial Doppler ultrasonography. T he subjects were nine awake volunteers (group A) and 18 patients receiving oral preanesthetic medication of clonidine, 3-4 mcg/kg, (group C), or place bo (group S). In groups C and S, anesthesia was induced with inhalation of sevoflurane-nitrous oxide. After tracheal intubation, anesthesia was mainta ined with 2% end-tidal sevoflurane alone, In group A, each volunteer wore a nose clip and breathed through a mouthpiece using a Mapleson D breathing s ystem. The time-mean middle cerebral artery flow velocity (Vmca) was measur ed during hypocapnia, normocapnia, and hypercapnia. In groups S and C, the Vmca values were significantly lower than those of g roup A at each PaCO2 level. The Vmca value of group C was significantly low er than that of group S in hypercapnia, but not in hypocapnia or normocapni a. The CO2 response slope of group C was significantly lower than those of groups A and S. The results indicate that clonidine, administered as an oral preanesthetic medication, reduces Vmca in hypercapnia but not in hypocapnia or normocapni a, and reduces the cerebrovascular CO2 response during sevoflurane anesthes ia.