The effects of dexmedetomidine on neuromuscular blockade in human volunteers

The neuromuscular effects of dexmedetomidine in humans are unknown. We eval uated the effect of dexmedetomidine on neuromuscular block and hemodynamics during propofol/alfentanil anesthesia. During propofol/alfentanil anesthes ia, the rocuronium infusion rate was adjusted in 10 volunteers to maintain a stable first response (T1) in the train-of-four sequence at 50% +/- 3% of the pre-rocuronium value. Dexmedetomidine was then administered by compute r-controlled infusion, targeting a plasma dexmedetomidine concentration of 0.6 ng/mL for 45 min. The evoked mechanical responses of the adductor polli cis responses (T1 response and T4/T1 ratio), systolic blood pressure (SBP), heart rate (HR), and transmitted light through a fingertip were measured d uring the dexmedetomidine infusion and compared with predexmedetomidine val ues using repeated-measures analysis of variance and Dunnett's test. Plasma dexmedetomidine levels ranged from 0.68 to 1.24 ng/mL. T1 values decreased during the infusion, from 51% +/- 2% to 44% +/- 9% (P < 0.0001). T4/T1 val ues did not change during the infusion. Plasma rocuronium concentrations in creased during the infusion (P = 0.02). Dexmedetomidine increased SEP (P < 0.001) and decreased HR (P < 0.001) (5-min median values) during the infusi on compared with values before the infusion. Dexmedetomidine increased the transmitted light through the fingertip by up to 41% +/- 8% during the dexm edetomidine infusion (P < 0.001). We demonstrated that dexmedetomidine (0.9 8 +/- 0.01 mu g/kg) increased the plasma rocuronium concentration, decrease d T1, increased SEP, and decreased finger blood flow during proyofol/alfent anil anesthesia. We conclude that dexmedetomidine-induced vasoconstriction may alter the pharmacokinetics of rocuronium. Implications: We studied the effect of an alpha(2)-agonist (dexmedetomidine) on rocuronium-induced neuro muscular block during propofol/alfentanil anesthesia. We found that the roc uronium concentration increased and the T1 response decreased during the de xmedetomidine administration. Although these effects were statistically sig nificant, it is unlikely that they are of clinical significance.