Eger Edmond I, Zhang Yi, Laster Michael, Flood Pamela, Kendig Joan J, Sonner James M
Department of Anesthesia and Perioperative Care, University of California, San Francisco, CA 94143-0464, USA.
Anesth Analg. 2002 Jun;94(6):1500-4, table of contents. doi: 10.1097/00000539-200206000-00023.
Acetylcholine receptors transmit excitatory impulses, are broadly distributed throughout the central nervous system, and are particularly sensitive to the depressant effects of inhaled anesthetics. Thus these receptors are potential mediators of the immobility produced by inhaled anesthetics. We tested this potential in rats by giving intraperitoneal atropine, scopolamine, and mecamylamine to block muscarinic (atropine and scopolamine) and neuronal nicotinic (mecamylamine) acetylcholine receptors. Block with scopolamine (up to 100 mg/kg), atropine (10 mg/kg), mecamylamine (up to 4 mg/kg), or atropine (10 mg/kg) plus mecamylamine (up to 4 mg/kg) did not significantly decrease the isoflurane concentration required to suppress movement to noxious stimulation (minimum alveolar anesthetic concentration). We also gave atropine intrathecally, finding that the infusions that did not cause permanent paralysis produced slight or no decreases in the minimum alveolar anesthetic concentration. We conclude that acetylcholine receptors do not seem to play a role as mediators of immobilization by inhaled anesthetics.
Inhaled anesthetics produce two crucial effects: amnesia and immobility in the face of noxious stimulation. Block of muscarinic and neuronal nicotinic acetylcholine receptors in rats does not significantly decrease the isoflurane concentration required to suppress movement to stimulation. Thus, acetylcholine receptors do not seem to play a major role as mediators of the immobilization produced by inhaled anesthetics. Their capacity to mediate other effects of inhaled anesthetics (e.g., amnesia) remains to be tested.
乙酰胆碱受体传递兴奋性冲动，广泛分布于中枢神经系统，并且对吸入麻醉药的抑制作用特别敏感。因此，这些受体是吸入麻醉药产生制动作用的潜在介质。我们通过腹腔注射阿托品、东莨菪碱和美加明来阻断毒蕈碱型（阿托品和东莨菪碱）和神经元烟碱型（美加明）乙酰胆碱受体，在大鼠中测试了这种可能性。用东莨菪碱（高达100mg/kg）、阿托品（10mg/kg）、美加明（高达4mg/kg）或阿托品（10mg/kg）加美加明（高达4mg/kg）进行阻断，并未显著降低抑制对有害刺激产生运动反应所需的异氟烷浓度（最低肺泡麻醉浓度）。我们还鞘内注射了阿托品，发现未引起永久性麻痹的注射对最低肺泡麻醉浓度产生了轻微降低或未产生降低。我们得出结论，乙酰胆碱受体似乎并非吸入麻醉药产生制动作用的介质。
吸入麻醉药产生两种关键作用：失忆和面对有害刺激时的制动。阻断大鼠的毒蕈碱型和神经元烟碱型乙酰胆碱受体，并未显著降低抑制对刺激产生运动反应所需的异氟烷浓度。因此，乙酰胆碱受体似乎并非吸入麻醉药产生制动作用的主要介质。它们介导吸入麻醉药其他作用（如失忆）的能力仍有待测试。
