Anesthetic and hemodynamic effects of dexmedetomidine during isoflurane anesthesia in a canine model.

Dexmedetomidine, an alpha 2-adrenergic agonist, was administered during isoflurane anesthesia to investigate its anesthetic sparing and hemodynamic effects in the canine model. Eleven healthy dogs were anesthetized with isoflurane, intubated, and allowed to breathe spontaneously. The animals were instrumented in order to measure or calculate mean arterial blood pressure (MABP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), cardiac output (CO), and systemic vascular resistance (SVR). Isoflurane minimum alveolar concentration (MAC), baseline hemodynamic measurements, and plasma catecholamine levels were determined. A 20 micrograms/kg bolus of dexmedetomidine was injected intravenously (IV) and MAC and hemodynamic values were redetermined. When isoflurane requirements were 33% of baseline, isoflurane was returned to 90% MAC and the alpha 2-antagonist, atipamezole, was administered. All dogs were treated with 40 micrograms/kg glycopyrrolate throughout the experiment to prevent any bradycardic response. Dexmedetomidine reduced isoflurane MAC by 86%. SVR, MABP, and LVEDP were significantly increased while CO and catechloamine levels were reduced. Atipamezole fully reversed the reduction in anesthetic requirements. MABP and catecholamine levels returned to baseline. SVR and LVEDP increased while CO decreased. The dogs exhibited a profound reduction in anesthetic requirement, reduced catecholamine levels, and changes in hemodynamic parameters with dexmedetomidine administration. The anesthetic sparing effect appears to be mediated by the alpha 2-receptor, since atipamezole reversed the reduction in MAC. Hemodynamic changes may be species or dose related, or due to differences in existing sympathetic tone. The role of dexmedetomidine warrants further study as an adjunct anesthetic agent.