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)