Oral dexmedetomidine attenuates hemodynamic responses during emergence from general anesthesia in chronically instrumented dogs.

Abstract

This investigation evaluated the hemodynamic effects of orally administered dexmedetomidine in chronically instrumented dogs in the conscious state, during enflurane anesthesia, and after emergence. Four experimental groups (n = 9 each) were completed. In groups 1 and 2, dexmedetomidine (10 or 20 micrograms/kg, respectively) was administered orally, and hemodynamics, arterial blood gas tensions, and plasma norepinephrine concentrations were monitored for 6 h. Animals in groups 3 and 4 were given dexmedetomidine (20 micrograms/kg) or placebo orally, and hemodynamics, arterial blood gas tensions, and plasma norepinephrine concentrations were measured 1 h later with animals in the conscious state, after 30 min of enflurane anesthesia (1.0 MAC), and 2 and 7 min after extubation. Oral administration of dexmedetomidine resulted in sedation with significant decreases in heart rate (76 +/- 4 to 49 +/- 4 beats per min), rate-pressure product (11,500 +/- 650 to 6,100 +/- 600 mmHg. beats per min), cardiac output (2.2 +/- 0.2 to 1.2 +/- 0.4 l/min), and plasma norepinephrine concentrations (290 +/- 50 to 135 pg/ml). Peak effects occurred within 30 min and lasted approximately 3 h. No reduction in coronary blood flow velocity, decrease in regional contractile function, or respiratory depression was observed. Administration of dexmedetomidine before enflurane anesthesia also was associated with a reduction in heart rate and rate-pressure product, and dexmedetomidine prevented the increase in heart rate (146 +/- 9 vs. 60 +/- 7 beats per min) and arterial pressure (117 +/- 7 vs. 98 +/- 7 mmHg) during emergence from anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)