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

2002 Fiscal Year Final Research Report Summary

• Project/Area Number: 13671568
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: KANAZAWA UNIVERSITY
• Principal Investigator: YAMAMOTO Ken KANAZAWA UNIVERSITY, POSTGRADUATE SCHOOL, PROFESSOR, 大学院・医学系研究科, 教授 (60135085)
• Co-Investigator(Kenkyū-buntansha): TSUBOKAWA Tsunehisa KANAZAWA UNIVERSITY, HOSPITAL, LECTUER, 医学部附属病院, 講師 (80283109)
• Project Period (FY): 2001 – 2002
• Keywords: High frequency oscillations / somatosensory evoked potentials / ketamine / sevoflurane / midazolam / gamma-aminobutyric acid

Research Abstract

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 cortex
1. 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 acceptable
2. Sevoflurane inhal 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 excitation
3. 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