Solt Ken, Eger Edmond I, Raines Douglas E
Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Anesth Analg. 2006 May;102(5):1407-11. doi: 10.1213/01.ane.0000204252.07406.9f.
N-Methyl-d-aspartate (NMDA) receptors have a presumed role in excitatory synaptic transmission and nociceptive pathways. Although previous studies have found that inhaled anesthetics inhibit NMDA receptor-mediated currents at clinically relevant concentrations, the use of different experimental protocols, receptor subtypes, and/or tissue sources confounds quantitative comparisons of the NMDA receptor inhibitory potencies of inhaled anesthetics. In the present study, we sought to fill this void by defining, using the two-electrode voltage-clamp technique, the extent to which diverse clinical and aromatic inhaled anesthetics inhibit the NR1/NR2B subtype of the human NMDA receptor expressed in Xenopus laevis oocytes. At 1 minimum alveolar anesthetic concentration (MAC), anesthetic compounds reversibly inhibited NMDA receptor currents by 12 +/- 6% to 74 +/- 6%. These results demonstrate that equianesthetic concentrations of inhaled anesthetics can differ considerably in the extent to which they inhibit NMDA receptors. Such differences may be useful for defining the role that this receptor plays in producing the in vivo actions of general anesthetics.
N-甲基-D-天冬氨酸（NMDA）受体在兴奋性突触传递和伤害性感受通路中可能发挥作用。尽管先前的研究发现，吸入麻醉药在临床相关浓度下可抑制NMDA受体介导的电流，但由于使用了不同的实验方案、受体亚型和/或组织来源，使得吸入麻醉药对NMDA受体抑制效能的定量比较变得复杂。在本研究中，我们试图通过使用双电极电压钳技术来确定多种临床用和芳香族吸入麻醉药对非洲爪蟾卵母细胞中表达的人NMDA受体NR1/NR2B亚型的抑制程度，以填补这一空白。在1个最低肺泡有效浓度（MAC）时，麻醉药化合物可使NMDA受体电流可逆性抑制12±6%至74±6%。这些结果表明，等效麻醉浓度的吸入麻醉药在抑制NMDA受体的程度上可能存在很大差异。这种差异可能有助于确定该受体在产生全身麻醉药体内作用中所起的作用。
