Schmeling W T, Ganjoo P, Staunton M, Drexler C, Farber N E
Department of Anesthesiology, The Medical College of Wisconsin, Milwaukee 53226, USA.
Anesth Analg. 1999 Mar;88(3):625-32. doi: 10.1097/00000539-199903000-00030.
The sedative and anesthetic-sparing ability of the alpha2-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 microg/kg p.o.). In both groups, four indices of anesthetic depth--minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to noxious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG isoelectricity)--were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3.14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis.
The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.
α2肾上腺素能激动剂右美托咪定的镇静和减少麻醉药用量的能力已有充分记录。在本研究中，我们确定了在慢性植入仪器的猫中，有或没有右美托咪定情况下，氟烷对血流动力学和脑电图（EEG）变量的影响，并量化了导致通过中枢神经系统（CNS）介导的各种麻醉深度指标的氟烷浓度。单独给予氟烷或在右美托咪定（15微克/千克口服）后给予氟烷。在两组中，测定了四个麻醉深度指标——最低肺泡麻醉浓度（MAC；对有害刺激无运动反应）、MAC（BAR）（对有害刺激无自主反应）、MAC（BS）（EEG爆发抑制）和MAC（等电位）（EEG等电位）。在爆发抑制和等电位出现之前，氟烷降低动脉血压、心率和EEG的高频成分。右美托咪定预处理增强了氟烷对动脉压、心率和EEG的作用。右美托咪定降低了导致MAC（从1.22%±0.06%降至0.89%±0.08%）和MAC（BAR）（从1.81%±0.05%降至1.1%±0.10%）的氟烷浓度，但未降低导致MAC（BS）（3.01%±0.17%对3.14%±0.10%）或MAC（等电位）（4.39%±0.26%对4.65%±0.12%）的氟烷浓度。这些结果表明，右美托咪定不会同等程度地改变各种CNS介导的麻醉作用指标，并且在神经轴的不同水平上存在不同程度的减少麻醉药用量的作用。
麻醉辅助药右美托咪定似乎会不同程度地改变中枢神经系统介导的麻醉作用指标。与较高脑功能（如脑电图）的指标相比，较低脑干或脊髓的麻醉深度决定因素（运动和血流动力学反应）受到的影响更大。
