Talke P O, Caldwell J E, Richardson C A, Kirkegaard-Nielsen H, Stafford M
Department of Anesthesia, University of California, San Francisco 94143-0648, USA.
Anesth Analg. 1999 Mar;88(3):633-9. doi: 10.1097/00000539-199903000-00031.
The neuromuscular effects of dexmedetomidine in humans are unknown. We evaluated the effect of dexmedetomidine on neuromuscular block and hemodynamics during propofol/alfentanil anesthesia. During propofol/alfentanil anesthesia, 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 computer-controlled infusion, targeting a plasma dexmedetomidine concentration of 0.6 ng/mL for 45 min. The evoked mechanical responses of the adductor pollicis responses (T1 response and T4/T1 ratio), systolic blood pressure (SBP), heart rate (HR), and transmitted light through a fingertip were measured during the dexmedetomidine infusion and compared with predexmedetomidine values 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 values did not change during the infusion. Plasma rocuronium concentrations increased during the infusion (P = 0.02). Dexmedetomidine increased SBP (P < 0.001) and decreased HR (P < 0.001) (5-min median values) during the infusion compared with values before the infusion. Dexmedetomidine increased the transmitted light through the fingertip by up to 41% +/- 8% during the dexmedetomidine infusion (P < 0.001).We demonstrated that dexmedetomidine (0.98 +/- 0.01 microg/kg) increased the plasma rocuronium concentration, decreased T1, increased SBP, and decreased finger blood flow during propofol/alfentanil anesthesia. We conclude that dexmedetomidine-induced vasoconstriction may alter the pharmacokinetics of rocuronium.
We studied the effect of an alpha2-agonist (dexmedetomidine) on rocuronium-induced neuromuscular block during propofol/alfentanil anesthesia. We found that the rocuronium concentration increased and the T1 response decreased during the dexmedetomidine administration. Although these effects were statistically significant, it is unlikely that they are of clinical significance.
右美托咪定对人体神经肌肉的影响尚不清楚。我们评估了右美托咪定在丙泊酚/阿芬太尼麻醉期间对神经肌肉阻滞和血流动力学的影响。在丙泊酚/阿芬太尼麻醉期间，对10名志愿者调整罗库溴铵输注速率，以维持四个成串刺激序列中的稳定强直后计数（T1）为罗库溴铵给药前值的50%±3%。然后通过计算机控制输注给予右美托咪定，目标血浆右美托咪定浓度为0.6 ng/mL，持续45分钟。在输注右美托咪定期间测量拇收肌的诱发机械反应（T1反应和T4/T1比值）、收缩压（SBP）、心率（HR）以及通过指尖的透射光，并使用重复测量方差分析和Dunnett检验与右美托咪定给药前的值进行比较。血浆右美托咪定水平范围为0.68至1.24 ng/mL。输注期间T1值下降，从51%±2%降至44%±9%（P<0.0001）。输注期间T4/T1值未改变。输注期间血浆罗库溴铵浓度升高（P = 0.02）。与输注前的值相比，右美托咪定在输注期间使SBP升高（P<0.001）并使HR降低（P<0.001）（5分钟中位值）。在右美托咪定输注期间，右美托咪定使通过指尖的透射光增加高达41%±8%（P<0.001）。我们证明，在丙泊酚/阿芬太尼麻醉期间，右美托咪定（0.98±0.01μg/kg）使血浆罗库溴铵浓度升高、T1降低、SBP升高并使手指血流减少。我们得出结论，右美托咪定诱导的血管收缩可能改变罗库溴铵的药代动力学。
我们研究了一种α₂激动剂（右美托咪定）在丙泊酚/阿芬太尼麻醉期间对罗库溴铵诱导的神经肌肉阻滞的影响。我们发现，在给予右美托咪定期间，罗库溴铵浓度升高且T1反应降低。尽管这些效应具有统计学意义，但它们不太可能具有临床意义。
