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J Neurosurg Anesthesiol · Jul 1999
Randomized Controlled Trial Clinical TrialEffects of clonidine on human middle cerebral artery flow velocity and cerebrovascular CO2 response during sevoflurane anesthesia.
- T Maekawa, S Cho, M Fukusaki, O Shibata, and K Sumikawa.
- Department of Anesthesiology, Nagasaki University School of Medicine, Japan.
- J Neurosurg Anesthesiol. 1999 Jul 1;11(3):173-7.
AbstractThe present study was designed to evaluate the effects of clonidine on human middle cerebral artery flow velocity and the cerebrovascular CO2 response during sevoflurane anesthesia using transcranial Doppler ultrasonography. The subjects were nine awake volunteers (group A) and 18 patients receiving oral preanesthetic medication of clonidine, 3-4 mcg/kg, (group C), or placebo (group S). In groups C and S, anesthesia was induced with inhalation of sevoflurane-nitrous oxide. After tracheal intubation, anesthesia was maintained 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 system. The time-mean middle cerebral artery flow velocity (Vmca) was measured during hypocapnia, normocapnia, and hypercapnia. In groups S and C, the Vmca values were significantly lower than those of group A at each PaCO2 level. The Vmca value of group C was significantly lower than that of group S in hypercapnia, but not in hypocapnia or normocapnia. 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 normocapnia, and reduces the cerebrovascular CO2 response during sevoflurane anesthesia.
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