Eger Edmond I, Xing Yilei, Laster Michael J, Sonner James M
Department of Anesthesia and Perioperative Care, University of California, San Francisco.
Anesth Analg. 2003 Jun;96(6):1661-1664. doi: 10.1213/01.ANE.0000061584.25288.98.
Agonism of alpha-adrenoreceptors has a powerful anesthetic result mediated, in part, by effects on the spinal cord. Alpha-adrenoreceptor agonists (e.g., dexmedetomidine) can decrease the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetics (e.g., halothane) to zero, with an apparently additive interaction between halothane and dexmedetomidine. We tested whether the capacity of the inhaled anesthetic isoflurane to produce immobility in the face of noxious stimulation resulted from agonism of alpha-adrenoreceptors. MAC (the concentration required to eliminate movement in response to a noxious stimulus in 50% of subjects) of isoflurane was determined before and after intraperitoneal administration of the alpha-adrenoreceptor antagonists yohimbine and atipamezole. The doses of yohimbine and atipamezole equaled or exceeded those that reverse the ability of agonism of alpha-adrenoreceptors to decrease MAC. Smaller doses of yohimbine or atipamezole slightly increased (by 10%) the MAC of isoflurane, an increase we interpret as the result of blockade of a small amount of tonically active alpha-adrenoreceptor activity. Doses five-fold larger did not change MAC. Doses 10-fold larger decreased MAC. We conclude that alpha-adrenoreceptors do not or minimally mediate the capacity of inhaled anesthetics to produce immobility.
Although stimulation (agonism) of alpha-2 adrenoreceptors can decrease the inhaled anesthetic concentration required to produce immobility in the face of noxious stimulation, blockade of alpha-2 adrenoreceptors minimally affects the concentration. Thus, augmentation of the effect of alpha-2 adrenoreceptors is not an appreciable part of the mechanism whereby inhaled anesthetics produce immobility.
α-肾上腺素能受体激动具有强大的麻醉效果，部分是通过对脊髓的作用介导的。α-肾上腺素能受体激动剂（如右美托咪定）可将吸入麻醉药（如氟烷）的最低肺泡有效浓度（MAC）降至零，氟烷与右美托咪定之间存在明显的相加作用。我们测试了吸入麻醉药异氟烷在面对有害刺激时产生不动状态的能力是否源于α-肾上腺素能受体激动。在腹腔注射α-肾上腺素能受体拮抗剂育亨宾和阿替美唑前后，测定异氟烷的MAC（使50%的受试者对有害刺激不产生运动反应所需的浓度）。育亨宾和阿替美唑的剂量等于或超过逆转α-肾上腺素能受体激动降低MAC能力的剂量。较小剂量的育亨宾或阿替美唑使异氟烷的MAC略有增加（10%），我们将这种增加解释为少量紧张性激活的α-肾上腺素能受体活性被阻断的结果。五倍大的剂量未改变MAC。十倍大的剂量降低了MAC。我们得出结论，α-肾上腺素能受体不介导或仅微弱介导吸入麻醉药产生不动状态的能力。
尽管刺激（激动）α2-肾上腺素能受体可降低在面对有害刺激时产生不动状态所需的吸入麻醉药浓度，但阻断α2-肾上腺素能受体对该浓度的影响极小。因此，增强α2-肾上腺素能受体的作用并非吸入麻醉药产生不动状态机制的重要组成部分。
