摘要
吸入麻醉药使人或动物对伤害性刺激不产生体动反应的具体机制，目前的研究仍然众说纷纭。一些研究发现，如吸入麻醉药之间的相加作用，提示各种麻醉药可能通过作用于一些共同的位点产生制动作用。然而，近20年来的研究却并未真正发现一种配体或是电压门控通道能单独介导这种制动作用。很多猜测的靶点，如阿片受体、5-HT3受体、GABA。受体、谷氨酸受体，以及钾和钙通道等，有的在制动效应的机制中仅起很小的作用，有的则完全没有作用。此外，多种配体门控通道或多种电压门控通道的联合效应也达不到这样的效果。少数较可信的靶点（如钠通道）值得进一步研究，但仍存在非特异性机制的可能。
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 inunobility. Indeed, most putative targets provide minimal or no mediation. For example, opioid, 5 -HT3, γ-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.
出处
《麻醉与镇痛》
2010年第3期61-78,共18页
Anesthesia & Analgesia
