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GENERAL ARTICLES

Dexmedetomidine Modulates Cardiovascular Responses to Stimulation of Central Nervous System Pressor Sites

Neil E. Farber, MD, PhD^*,,,§, Enric Samso, MD, PhD^*, Michael Staunton, MB, FFARCSI^*, David Schwabe, BS^*, and William T. Schmeling, 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 William T. Schmeling, MD, PhD, Medical College of Wisconsin, MEB, 462C, 8701 Watertown Plank Rd., Milwaukee, WI 53226. Address e-mail to willie{at}mcw.edu

Halothane attenuates the alterations in arterial pressure (BP) and heart rate (HR) produced by central nervous system (CNS) stimulation. We examined the effects of the ₂-adrenergic agonist dexmedetomidine, with and without halothane, on cardiovascular regulation during CNS pressor site stimulation in chronically instrumented cats. Stimuli trains via bipolar stimulating electrodes in the hypothalamus and reticular formation elicited pressor responses. Dexmedetomidine-induced (15 µg/kg PO) bradycardia was greater in the presence of halothane. CNS stimulation increased BP and HR, which were dose-dependently attenuated by halothane (hypothalamic stimulation 71 ± 9 mm Hg at control, 25 ± 5 and 15 ± 3 mm Hg at 1.0% and 1.5% halothane, respectively). Although dexmedetomidine alone did not alter pressor responses, halothane plus dexmedetomidine attenuated pressor responses in a potentially synergistic fashion (hypothalamic stimulation 67 ± 8 mm Hg at control, 2 ± 1 and 1 ± 0.4 mm Hg at 1.0% and 1.5% halothane, respectively). These results suggest differences in the disruptive effects of CNS-mediated cardiovascular responses by halothane and dexmedetomidine, and that dexmedetomidine has an anesthetic-sparing effect on these CNS-mediated cardiovascular control mechanisms, potentiating the depressant effect of halothane.

Implications: A new potential anesthetic adjunct, dexmedetomidine, does not attenuate brain-mediated increases in blood pressure, but the combination of dexmedetomidine and the anesthetic halothane acts to modulate central cardiovascular responses.

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