Eger Edmond I, Raines Douglas E, Shafer Steven L, Hemmings Hugh C, Sonner James M
Department of Anesthesia and Perioperative Care, University of California, San Francisco, California 94143-0464, USA.
Anesth Analg. 2008 Sep;107(3):832-48. doi: 10.1213/ane.0b013e318182aedb.
A paradox arises from present information concerning the mechanism(s) by which inhaled anesthetics produce immobility in the face of noxious stimulation. Several findings, such as additivity, suggest a common site at which inhaled anesthetics act to produce immobility. However, two decades of focused investigation have not identified a ligand- or voltage-gated channel that alone is sufficient to mediate immobility. Indeed, most putative targets provide minimal or no mediation. For example, opioid, 5-HT3, gamma-aminobutyric acid type A and glutamate receptors, and potassium and calcium channels appear to be irrelevant or play only minor roles. Furthermore, no combination of actions on ligand- or voltage-gated channels seems sufficient. A few plausible targets (e.g., sodium channels) merit further study, but there remains the possibility that immobilization results from a nonspecific mechanism.
关于吸入麻醉药在面对有害刺激时产生制动作用的机制，目前的信息引发了一个悖论。一些研究结果，如相加性，表明吸入麻醉药产生制动作用存在一个共同作用位点。然而，二十年的重点研究尚未确定单独足以介导制动作用的配体门控或电压门控通道。实际上，大多数假定的靶点仅提供极少的介导作用或根本没有介导作用。例如，阿片类、5-羟色胺3型、A型γ-氨基丁酸和谷氨酸受体，以及钾通道和钙通道似乎无关紧要或仅起次要作用。此外，对配体门控或电压门控通道的任何联合作用似乎都不足以产生制动作用。一些看似合理的靶点（如钠通道）值得进一步研究，但制动作用仍有可能是由非特异性机制导致的。
