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

Authors:
  • NFNeil E. Farber
    Neil E. Farber
  • ESEnric Samso
    Enric Samso
  • MSMichael Staunton
    Michael Staunton
  • DSDavid Schwabe
    David Schwabe
  • WSWilliam T. Schmeling
    William T. Schmeling

Abstract
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 alpha2-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 [micro sign]g/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. (Anesth Analg 1999;88:617-24)

This publication has 21 references indexed in Scilit: