Pretreatment with dexmedetomidine: Altered indices of anesthetic depth forhalothane in the neuraxis of cats

The sedative and anesthetic-sparing ability of the alpha(2)-adrenergic agon ist dexmedetomidine is well documented. Ln this study, we identified the ef fects of halothane, with and without dexmedetomidine, on hemodynamic and el ectroencephalographic (EEG) variables and quantified the concentration of h alothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane w as given alone or after dexmedetomidine (15 mu g/kg PO). In both groups, fo ur indices of anesthetic depth-minimum alveolar anesthetic concentration (M AC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to nox ious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG i soelectricity)-were determined. Halothane decreased arterial blood pressure , heart rate, and higher frequency components of the EEG before the onset o f burst suppression and isoelectricity. Dexmedetomidine pretreatment augmen ted the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (fro m 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3. 14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). Th ese results suggest that dexmedetomidine does not alter various CNS-mediate d indices of anesthetic action to equivalent degrees and that there are dis similar degrees of an anesthetic-sparing action at different levels of the neuraxis. Implications: The anesthetic adjuvant dexmedetomidine seems to di fferentially alter central nervous system-mediated indices of anesthetic ac tion. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain f unctions, such as the electroencephalogram.