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GENERAL ARTICLES

Pretreatment with Dexmedetomidine: Altered Indices of Anesthetic Depth for Halothane in the Neuraxis of Cats

William T. Schmeling, MD, PhD^*,,||, Pragati Ganjoo, MBBS, DA, DNB^*, Michael Staunton, MB, FFARCSI^*, Cathy Drexler, MD^*, and Neil E. Farber, MD, PhD^*,,,§

Departments of *Anesthesiology, Pediatrics, and Pharmacology & Toxicology, The Medical College of Wisconsin; §Children’s Hospital of Wisconsin; and the ||Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin;

Address correspondence and reprint requests to Neil E. Farber, MD, PhD, Department of Anesthesiology, Medical College of Wisconsin, MEB 462C, 8701 Watertown Plank Rd., Milwaukee, WI 53226. Address e-mail to nfarber{at}mcw.edu

The sedative and anesthetic-sparing ability of the ₂-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 µg/kg PO). In both groups, four indices of anesthetic depth—minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC_BAR (no autonomic response to noxious stimuli), MAC_BS (EEG burst suppression), and MAC_ISOELECTRIC (EEG isoelectricity)—were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 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%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis.

Implications: The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.

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				B.-H. Li, J. S. Lohmann, H. G. Schuler, and A. J. Cronin Preservation of the Cortical Somatosensory-Evoked Potential During Dexmedetomidine Infusion in Rats Anesth. Analg., April 1, 2003; 96(4): 1155 - 1160. [Abstract] [Full Text] [PDF]

				N. E. Farber, E. Samso, M. Staunton, D. Schwabe, and W. T. Schmeling Dexmedetomidine Modulates Cardiovascular Responses to Stimulation of Central Nervous System Pressor Sites Anesth. Analg., March 1, 1999; 88(3): 617 - 617. [Abstract] [Full Text] [PDF]