Duarte Leonardo Teixeira Domingues, Saraiva Renato Angelo
Rede Sarah de Hospitais do Aparelho Locomotor.
Rev Bras Anestesiol. 2005 Feb;55(1):100-17. doi: 10.1590/s0034-70942005000100013.
Immobility is an essential component of general anesthesia and should be looked for and maintained throughout anesthesia. Anesthetic potency, called Minimum Alveolar Concentration (MAC), results from the inhibition of movement response to noxious stimulation. However, although spinal cord is recognized as the primary mediator of surgical immobility, cellular and subcelular mechanisms of action of inhaled anesthetics to produce immobility are not yet totally known. Considering major research advances on mechanisms of action of inhaled anesthetics and resulting wide variety of information, this review aimed at critically evaluating clinical and experimental studies performed to identify sites of action and mechanisms of inhaled anesthetics to promote immobility in response to noxious stimulations.
Complex mechanisms of action of inhaled anesthetics on central nervous system may be divided into three levels: macroscopic, microscopic, and molecular. Macroscopically, behavioral studies have shown spinal cord to be the primary anesthetic site of action to promote immobility in response to noxious stimulations. At cellular level, excitability of motor neurons, nociceptive neurons and synaptic transmission are involved in the anesthetic action. At molecular level, several receptors are affected by inhaled anesthetics, but only a few may directly mediate anesthetic action, among them: glycine, glutamate AMPA and 5-HT2A receptors, in addition to voltage-gated sodium channels.
Inhaled anesthetics-induced immobility is primarily mediated by an action on the spinal cord, as a consequence of anesthetic action upon motor neurons excitability and upon nociceptive neurons of the spinal cord dorsal horn. Actions on specific receptors have an effect on their synaptic transmission.
制动是全身麻醉的一个重要组成部分，在整个麻醉过程中都应予以关注并维持。麻醉效能，即所谓的最低肺泡浓度（MAC），源于对有害刺激的运动反应受到抑制。然而，尽管脊髓被认为是手术制动的主要介导者，但吸入麻醉药产生制动作用的细胞和亚细胞作用机制尚未完全明确。鉴于吸入麻醉药作用机制方面的重大研究进展以及由此产生的大量信息，本综述旨在批判性地评估为确定吸入麻醉药在应对有害刺激时促进制动的作用部位和机制而进行的临床和实验研究。
吸入麻醉药对中枢神经系统的复杂作用机制可分为三个层面：宏观层面、微观层面和分子层面。在宏观层面，行为学研究表明脊髓是吸入麻醉药在应对有害刺激时促进制动的主要作用部位。在细胞水平，运动神经元、伤害性神经元的兴奋性以及突触传递都参与了麻醉作用。在分子水平，几种受体受吸入麻醉药影响，但其中只有少数可能直接介导麻醉作用，包括：甘氨酸、谷氨酸AMPA和5-HT2A受体，以及电压门控钠通道。
吸入麻醉药诱导的制动主要是通过对脊髓的作用介导的，这是由于麻醉药作用于运动神经元兴奋性以及脊髓背角的伤害性神经元。对特定受体的作用会影响其突触传递。
