Effects of general anesthetics on substance P release and c-Fos expression in the spinal dorsal horn

我们检测了全麻对福尔马林诱导的P物质释放和背角表面c-Fos表达的影响。芬太尼，而非异丙酚、戊巴比妥、异氟醚或氧化亚氮单独抑制NK1受体内化（NK1Ri）。而异氟烷+氧化亚氮能还原NK1Ri。所有药物均降低了c-Fos在浅表背角的表达。麻醉浓度的全麻通过一种独立于对初级传入肽释放的影响的机制来阻断脊髓神经元的激活。芬太尼的单独作用以及异氟醚和氧化亚氮对P物质释放的协同作用表明，这些麻醉方案的治疗用途是通过阻断伤害性传入递质的释放和防止突触后直接到初级传入的级联反应的开始。

We examined the effects of general anesthetics on formalin-induced substance P release and c-Fos expression in superficial dorsal horn. Fentanyl, but not propofol, pentobarbital, isoflurane nor nitrous oxide alone inhibited NK1 receptor internalization (NK1Ri). However, isoflurane+nitrous oxide reduced NK1Ri. All agents reduced c-Fos expression in the superficial dorsal horn.General anesthetics at anesthetic concentrations block spinal neuronal activation through a mechanism which is independent of an effect upon small primary afferent peptide release. The effect of fentanyl alone and the synergistic effect of isoflurane and nitrous oxide on substance P release suggests a correlative rationale for the therapeutic use of these anesthetic protocol by blocking nociceptive afferent transmitter release and preventing the initiation of cascade which are immediately postsynaptic to the primary afferent.