Cardiovascular and parasympathetic effects of dexmedetomidine in healthy subjects

Abstract

We evaluated the cardiovascular effects of intravenously (i.v.) and buccally administered dexmedetomidine, a selective α2-adrenoceptor agonist. Six healthy male subjects were studied unmedicated and after 2 µg/kg i.v. or buccal doses of dexmedetomidine, using repeated recordings of ECG and blood pressure. Cardiac parasympathetic activity was estimated by measurements of high-frequency (HF) heart rate variability. Intravenous, but not buccal, dexmedetomidine raised systolic blood pressure by 11 ± 5 mmHg (mean ± SEM) and diastolic by 16 ± 3 mmHg (maxima at 10 min). Later on, both i.v., and buccal dexmedetomidine produced a very similar hypotensive effect: on average, [Formula: see text]10 mmHg reductions in systolic and diastolic pressure at 3 h. Intravenous dosing was followed by a decline in heart rate (–11 ± 2 beats/min) accompanied by a trend toward enhanced HF variability (maximal effect at 10 min), which probably reflected baroreflex-mediated parasympathetic efferent neuronal activation. Buccal dexmedetomidine increased significantly the HF variability (maximum at 45 min) without influencing heart rate. We conclude that dexmedetomidine, when administered by a method that avoids concentration peaks, e.g., buccal dosing, can be used to produce a prolonged augmentation of cardiac parasympathetic efferent neuronal activity.Key words: dexmedetomidine, parasympathetic nervous system, heart rate, blood pressure.