Basic and Clinical research about High Frequency Oscillations (600 Hz)

高频振荡（hfo）是由数字带通滤波器从体感诱发电位（sep）中分离出来的尖峰状小波的爆发。SEPs是由大脑皮层锥体细胞产生的，而hfo则反映了抑制性中间神经元的活动。一种假说认为，麻醉药物通过增强γ -氨基丁酸（GABA）的作用来启动麻醉作用。因此，我们研究了七氟醚和咪达唑仑对sep和hfo的影响。Wistar雄性大鼠坐骨神经直接电刺激诱发的sep和HFOs在躯体感觉皮层均有记录。首先，我们检查氯胺酮输注是否适合本研究的麻醉方法。氯胺酮的镇痛作用经热辐射种植试验证实，但sep和hfo的潜伏期和剂量依赖性增加没有变化。我们认为氯胺酮输注是可接受的2。多吸入七氟醚可延长sep潜伏期，并引起特征性的双相振幅变化；低浓度的七氟醚增加了SEPs的振幅；高浓度的七氟醚剂量依赖性地降低了振幅。这一现象可以解释为：低浓度的七氟醚仅作用于皮质水平的GABA受体，由于GABA停止向树突转移，锥体细胞的兴奋可以到达皮质表面而不衰减。另一方面，高浓度的七氟醚不仅作用于皮质，而且作用于丘脑的GABA受体，并减少传入兴奋的量3。咪达唑仑延长了sep和hfo的潜伏期，且两个峰的潜伏期延长长度相等。早期sep的振幅没有变化，而晚期sep的振幅有所下降。相反，所有hfo的峰值幅度都明显减小。咪达唑仑的作用部位被认为在丘脑或低于丘脑

High frequency oscillations (HFOs) are a burst of spike-like wavelets separated from somatosensory evoked potentials (SEPs) by digital bandpass filters. SEPs are generated by pyramidal cells in the cerebral cortex, while HFOs reflect activities of inhibitory interneurons. One hypothesis states that anesthetic drugs initiate anesthetic action by, enhancement of gamma-aminobutyric acid (GABA) action. Therefore, we investigated the effect of sevoflurane and midazolam on SEPs and HFOs. In Wistar male rats, SEPs and HFOs evoked by direct electric stimulation of the ischiatic nerve were recorded in the soma tosensory cortex1. First, we examined whether ketamine infusion was an appropriate anesthetic method for this investigation. The analgesic effect of ketamine was certified by a planter test with heat radiation, while s bowing no change in the latencies and dose dependently increasing of the amplitudes of SEPs and HFOs. We concluded that ketamine infusion was acceptable2. Sevoflurane inhal … More ation prolonged the latency of SEPs, and caused characteristic biphasic changes of amplitude ; a low concentration of sevoflurane increased the amplitude of SEPs ; a high concentration of sevoflurane decreased the amplitude dose dependently. This phenomenon can be explained as follows : a low concentration of sevoflurane acts on only the cortical level GABA receptors, as a result, excitation of the pyramidal cells could reach the surface of the cortex without decay, because GABA stops diverting flow to dendrites. On the other hand, a high concentration of sevoflurane acts on not only the cortical but also thalamic GABA receptors, and it decreases the amount of afferent excitation3. Midazolam prolonged the latencies of SEPs and HFOs, and the length of prolonged latencies was equal at each peak. The amplitudes of early SEPs did not show any change, whereas those of late S EPs decreased. On the contrary, the amplitudes of all HFOs' peaks were markedly decreased. The action site of midazolam is assumed to be in the thalamus or below it Less