The effect of neuroleptanalgesia (droperiodol-fentanyl) on motor potentials evoked by transcranial magnetic stimulation in the monkey.

The effect of neuroleptanalgesia (droperiodol-fentanyl) on motor potentials evoked by transcranial magnetic stimulation in the monkey.
复制标题

神经乐普镇痛(滴周期醇-芬太尼)对经颅磁刺激诱发的猴子运动电位的影响。

DOI:
10.1097/00008506-199106000-00006
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发表时间:
1991
影响因子:
3.7
通讯作者:
Ralf Laege
Ralf Laege
中科院分区:
医学3区
文献类型:
--
作者:
R. Ghaly;James L. Stone;Walter J. Levy;R. Kartha;Edward A. Brunner;J. Aldrete;Ralf Laege

文献摘要

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本文对12只猴在神经安定镇痛(NLA)状态下经颅磁刺激(TMS)后的运动诱发电位(MEP)进行了研究。在刺激部位对侧的拇短展肌(APB)和腓肠肌(GN)记录复合肌肉动作电位。在从10 mg/kg肌肉注射的美索己酮苏醒期间获得基线描记后,NLA诱导使用droperiodol,0.3 mg/kg静脉注射,然后芬太尼,0.006 mg/kg静脉注射。连续MEP记录后10分钟静脉注射droperiodol,2,8,和16分钟静脉注射芬太尼,并在恢复期间。在NLA下一致记录了可重复的TMS MEP。然而,与对照值相比,氟哌利多和芬太尼引起显著的刺激阈值升高、振幅降低和潜伏期延迟(p <0.01)。氟碘油给药后10分钟,APB-GN阈值、振幅和潜伏期值(平均值+/- SD)为0.81 +/- 0.2-0.84 +/- 0.1 T(基线0.57 ± 0.1-0.59 ± 0.1 T),3.4 ± 2.1-4.0 ± 2.5 mV(基线8.0 +/- 3.7-9.0 +/- 3.7 mV)和15.8 +/- 1.3-21.1 +/- 1.2 ms(基线14.9 +/- 1.2-20.1 +/- 1.3 ms)。芬太尼的加入导致反应进一步恶化。芬太尼注射后2分钟,APB-GN阈值、振幅和潜伏期值分别为0.88 +/- 0.18- 0.95%% 0.15 T、2.1 +/- 1.7-2.0 +/- 2.1 mV和16.0 +/- 1.4-21.9 +/- 1.3 ms。随后的MEP显示反应逐渐改善,但与基线相比,仍显着改变(p <0.05)。在恢复期(53 +/- 6 min),APB-GN阈值、振幅和潜伏期测量值分别为0.66 +/- 0.1-0.77 +/- 0.2 T、4.4 +/- 3.1-4.2 +/- 2.9 mV、15.5%% 1.4-20.9 +/- 1.7 ms。我们的结论是,在灵长类动物模型中,NLA保持可测量的TMS MEP。然而,氟碘油和芬太尼产生显著和长期的反应改变。术中给予NLA药物时,了解这些变化对于解释MEP数据至关重要。
Motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) have been examined in 12 monkeys under neuroleptanalgesia (NLA). Compound muscle action potentials were recorded from abductor policis brevis (APB) and gastroncnemius (GN) muscles contralateral to the stimulation site. After obtaining baseline tracings during emergence from methohexitone, 10 mg/kg i.m., NLA was induced using droperiodol, 0.3 mg/kg i.v. followed by fentanyl, 0.006 mg/kg i.v. Sequential MEP recordings were obtained 10 min after i.v. droperiodol, 2, 8, and 16 min after i.v. fentanyl, and during recovery. Replicable TMS MEPs were consistently recorded under NLA. However, droperidol and fentanyl caused significant stimulation threshold elevation, amplitude depression, and latency delay compared to control values (p <0.01). Ten minutes after droperiodol administration, the APB-GN threshold, amplitude, and latency values (mean +/- SD) were 0.81 +/- 0.2-0.84 +/- 0.1 T (baseline 0.57 +/- 0.1-0.59 +/- 0.1 T), 3.4 +/- 2.1-4.0 +/- 2.5 mV (baseline 8.0 +/- 3.7-9.0 +/- 3.7 mV), and 15.8 +/- 1.3-21.1 +/- 1.2 ms (baseline 14.9 +/- 1.2-20.1 +/- 1.3 ms), respectively. Addition of fentanyl resulted in further response deterioration. Two minutes after fentanyl injection, the APB-GN threshold, amplitude, and latency values were 0.88 +/- 0.18-0.95 %% 0.15 T, 2.1 +/- 1.7-2.0 +/- 2.1 mV, and 16.0 +/- 1.4-21.9 +/- 1.3 ms, respectively. Subsequent MEPs revealed gradual response improvement but, in contrast to baseline, remained markedly altered (p <0.05). During the recovery period (53 +/- 6 min), the APB-GN threshold, amplitude, and latency measurements were 0.66 +/- 0.1-0.77 +/- 0.2 T, 4.4 +/- 3.1-4.2 +/- 2.9 mV, 15.5 %% 1.4-20.9 +/- 1.7 ms, respectively. We conclude that, in a primate model, NLA maintains measurable TMS MEPs. Nevertheless, droperiodol and fentanyl produce significant and prolonged response alterations. Knowledge of these changes, while administering NLA drugs intraoperatively, is essential to interpretation of MEP data.