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【第365篇】多巴胺D1受体活化促进异氟烷全身麻醉苏醒 Anesthesiology.2013 Jan;118(1):30-39.

Activation of D1 Dopamine Receptors Induces Emergence from Isoflurane General Anesthesia.

Taylor NE, Chemali JJ, Brown EN, Solt K.

* Clinical Fellow, Department of Anaesthesia, Harvard Medical School, Boston, Massachusetts, and Resident, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts. ? Research Assistant, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital. ? Anesthetist, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital; Warren M. Zapol Professor, Department of Anaesthesia, Harvard Medical School; Professor of Computational Neuroscience, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts; Professor of Health Sciences and Technology, Institute for Medical Engineering and Science, Massachusetts Institute of Technology. § Assistant Professor, Department of Anaesthesia, Harvard Medical School; Assistant Anesthetist, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital; and Research Affiliate, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology.

Abstract

BACKGROUND: A recent study showed that methylphenidate induces emergence from isoflurane anesthesia. Methylphenidate inhibits dopamine and norepinephrine reuptake transporters. The objective of this study was to test the hypothesis that selective dopamine receptor activation induces emergence from isoflurane anesthesia.

METHODS:

In adult rats, we tested the effects of chloro-APB (D1 agonist) and quinpirole (D2 agonist) on time to emergence from isoflurane general anesthesia. We then performed a dose-response study to test for chloro-APB-induced restoration of righting during continuous isoflurane anesthesia. SCH-23390 (D1 antagonist) was used to confirm that the effects induced by chloro-APB are specifically mediated by D1 receptors. In a separate group of animals, spectral analysis was performed on surface electroencephalogram recordings to assess neurophysiologic changes induced by chloro-APB and quinpirole during isoflurane general anesthesia.

RESULTS: Chloro-APB decreased median time to emergence from 330 to 50 s. The median difference in time to emergence between the saline control group (n = 6) and the chloro-APB group (n = 6) was 222 s (95% CI: 77-534 s, Mann-Whitney test). This difference was statistically significant (P = 0.0082). During continuous isoflurane anesthesia, chloro-APB dose-dependently restored righting (n = 6) and decreased electroencephalogram δ power (n = 4). These effects were inhibited by pretreatment with SCH-23390. Quinpirole did not restore righting (n = 6) and had no significant effect on the electroencephalogram (n = 4) during continuous isoflurane anesthesia.

CONCLUSIONS: Activation of D1 receptors by chloro-APB decreases time to emergence from isoflurane anesthesia and produces behavioral and neurophysiologic evidence of arousal during continuous isoflurane anesthesia. These findings suggest that selective activation of a D1 receptor-mediated arousal mechanism is sufficient to induce emergence from isoflurane general anesthesia.

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多巴胺D1受体活化促进异氟烷全身麻醉苏醒

背景：最近的一项研究表明哌醋甲酯促进异氟烷全身麻醉苏醒。哌醋甲酯能够抑制多巴胺和去甲肾上腺素的再摄取。本研究旨在验证选择性活化多巴胺受体可促进异氟烷全身麻醉苏醒的假说。

方法：在成年大鼠中，我们检测多巴胺D1受体激动剂（chloro-APB）和D2受体激动剂（quinpirole）对异氟烷全身麻醉苏醒时间的影响。然后，我们对chloro-APB促进持续异氟烷全身麻醉大鼠翻正反射恢复的作用进行剂量相关性研究。D1受体抑制剂（SCH-23390）用于证实chloro-APB通过选择性作用于D1受体发挥促进苏醒的作用。在单独一组动物中，我们对记录到的脑电图进行频谱分析，进而评价在持续异氟烷全身麻醉时chloro-APB和quinpirole对神经生理学影响。

结果：chloro-APB将苏醒中位时间从330s降低到50s。生理盐水组（n=6）和chloro-APB组（n=6）苏醒时间差值的中位数为222s（95% 可信区间: 77-534 s, Mann-Whitney test）。差异具有统计学意义（p=0.0082）。在异氟烷持续麻醉时，chloro-APB剂量依赖性促进翻正反射恢复（n=6）和减少δ 脑电波的活动（n=4）。通过SCH-23390预处理可抑制该作用。在异氟烷持续麻醉时，Quinpirole组未出现翻正反射恢复（n=6）及对脑电图无明显影响（n=4）。

结论：D1受体活化减少异氟烷全身麻醉的苏醒时间，觉醒行为学和神经生理学的证据表明其在异氟烷持续全身麻醉时能够促进觉醒。这些发现提示，选择性激活D1受体足以导致异氟烷全身麻醉的苏醒。