McAdam L C, MacDonald J F, Orser B A
Anaesthesia Research Laboratory, University of Toronto, Ontario, Canada.
Anesthesiology. 1998 Dec;89(6):1444-54. doi: 10.1097/00000542-199812000-00022.
Clinical studies suggest that midazolam and propofol interact synergistically to induce hypnosis, but these drugs do not interact synergistically to prevent movement in response to noxious stimuli. The mechanisms underlying these interactions are not certain but may occur at the level of the gamma-aminobutyric acid A (GABA(A)) receptor.
The authors evaluated the interactions between propofol and midazolam in modulating GABA(A) receptor activity in embryonic hippocampal neurons. The effects of midazolam and propofol on peak current evoked by submaximal concentrations of GABA were studied using the patch clamp method. Isobolographic analysis was undertaken by constructing concentration-response curves for midazolam and propofol alone and then evaluating the potency of combinations of midazolam and propofol. In other experiments, the concentration of GABA was increased and flurazepam was substituted for midazolam.
Isobolographic analysis confirmed that midazolam and propofol interact synergistically to enhance currents evoked by low concentrations of GABA (1 microM). However, when the concentration of GABA was increased to 3 microM, the interaction was additive. The interaction between flurazepam and propofol was also additive for enhancement of currents evoked by 3 microM GABA.
The interaction between midazolam and propofol was critically dependent on the concentration of GABA: Synergism was evident at low concentrations of GABA, but an additive interaction was apparent when the concentration of GABA was increased. Changes in GABA(A) receptor function may underlie the synergistic interaction between propofol and midazolam for clinical effects such as hypnosis. The clinical implication of the results is that the benefits of synergism observed at one concentration ratio of these drugs may not be apparent at another.
临床研究表明,咪达唑仑和丙泊酚相互协同作用以诱导催眠,但这些药物在预防对有害刺激的反应性运动方面并无协同作用。这些相互作用的潜在机制尚不确定,但可能发生在γ-氨基丁酸A(GABAA)受体水平。
作者评估了丙泊酚和咪达唑仑在调节胚胎海马神经元GABAA受体活性方面的相互作用。使用膜片钳方法研究了咪达唑仑和丙泊酚对亚最大浓度GABA诱发的峰值电流的影响。通过构建咪达唑仑和丙泊酚单独的浓度-反应曲线,然后评估咪达唑仑和丙泊酚组合的效价,进行了等效线分析。在其他实验中,增加了GABA的浓度,并用氟西泮替代了咪达唑仑。
等效线分析证实,咪达唑仑和丙泊酚相互协同作用以增强低浓度GABA(1微摩尔)诱发的电流。然而,当GABA浓度增加到3微摩尔时,这种相互作用是相加的。氟西泮和丙泊酚之间的相互作用在增强3微摩尔GABA诱发的电流方面也是相加的。
咪达唑仑和丙泊酚之间的相互作用严重依赖于GABA的浓度:在低浓度GABA时协同作用明显,但当GABA浓度增加时相加相互作用明显。GABAA受体功能的变化可能是丙泊酚和咪达唑仑在催眠等临床效应方面协同相互作用的基础。这些结果的临床意义在于,在这些药物的一种浓度比下观察到的协同作用益处,在另一种浓度比下可能并不明显。