Dexmedetomidine and halothane produce similar alterations in electroencephalographic and electromyographic activity in cats.

Dexmedetomidine, an alpha2-adrenergic agonist, produces sedation and reduces volatile anesthetic requirements. This investigation compared the actions of dexmedetomidine and halothane on the processed EEG and on the electromyogram (EMG) which has not been previously described. Chronically instrumented cats were prepared with arterial and venous cannulae, quadriceps EMG electrodes and EEG electrodes in the lateral geniculate nucleus and over the frontal and occipital cortices. Hemodynamics, EEG and EMG were recorded in the conscious state and after randomly administered halothane or intravenous dexmedetomidine (on separate days). Blink and tail-clamp responses also assessed level of consciousness. Halothane resulted in unconsciousness and a lack of response to tail clamping, while dexmedetomidine produced profound sedation, with preservation of tail-clamp responses. Both agents similarly decreased (P < 0.05) the median power frequency from 9.5 +/- 0.9 to 5.7 +/- 0.4 Hz (2% halothane) and from 9.6 +/- 0.7 to 5.9 +/- 0.8 Hz (20 microg/kg dexmedetomidine), and 95% power frequency from 23.0 +/- 0.2 to 18.2 +/- 0.6 Hz (2% halothane) and from 23.0 +/- 0.2 to 19.1 +/- 0.8 Hz (20 microg/kg dexmedetomidine). Both agents increased the total spectral power and delta band power of the EEG and reduced integrated EMG activity. Halothane and dexmedetomidine produced differing effects on level of consciousness as assessed by response to tail clamping. The results suggest that conventional processing of EEG and EMG parameters are inadequate to assess anesthetic depth in the presence of alpha2-adrenergic agonists.