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Autonomic Nervous System

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Responses of higher brain function and ventilation to mild and severe hypoxia

  • P1-197
  • 武田 湖太郎 / Kotaro Takeda:1,2 福士 勇人 / Isato FUKUSHI:2,3,4 國谷 真由 / Mayu KUNIYA:5 長谷部 洋平 / Youhei Hasebe:2,6 村岡 慶裕 / Yoshihiro MURAOKA:2,5 堀内 城司 / Jouji Horiuchi:3 岡田 泰昌 / Yasumasa Okada:2 
  • 1:藤田保健衛生大学・藤田記念七栗研究所 / Fujita Memorial Nanakuri Institute, Fujita Health University, Mie, Japan 2:国立病院機構村山医療センター・臨床研究センター / Clinical Research Center, National Hospital Organization Murayama Medical Center, Tokyo, Japan 3:東洋大学・大学院・理工学研究科・生体医工学科 / Department of Biomedical Engineering, Graduate School of Science and Engineering, Toyo University, Saitama, Japan 4:デンタルサポート株式会社 / Planning Division, Dental Support Co., Ltd., Chiba, Japan 5:早稲田大学・人間科学部 / School of Human Sciences, Waseda University, Saitama, Japan 6:山梨大学・医学部・小児科学講座 / Department of Pediatrics, School of Medicine, University of Yamanashi, Yamanashi, Japan 

Although respiratory motor output is controlled in the brainstem, ventilation and its responses to hypoxia are also dependent on the higher brain status. In the present study, we aimed to explore the relationship between the higher brain function and ventilatory responses to mild and severe hypoxia. We simultaneously analyzed the higher brain status and ventilatory parameters in unanesthetized adult mice by EEG and whole body plethysmography, respectively. Screw electrodes for EEG recording were secured in the skull, which targeted at 2.5 mm anterior and 2.5 mm posterior to the bregma. Two-channel EEG signals from the anterior and posterior electrodes were recorded at 400 Hz sampling, and bandpass filtered at 0.1-100 Hz. Digital power spectrogram was generated by a fast Fourier transform from the filtered EEG waveform, and its respiration-triggered averaging was performed. In whole body plethysmography, respiratory flow was measured at 400 Hz sampling and bandpass filtered at 0.1-20 Hz. We then calculated tidal volume, respiratory rate and minute ventilation. For the analysis of ventilatory responses to hypoxia, mice breathed first room air, then mild (12% O2 in N2) or severe (6% O2 in N2) hypoxic gas, and again room air. In the room air condition, EEG signals recorded from the anterior electrodes were respiration-synchronized, but those from the posterior electrodes were not. Mild hypoxia persistently increased ventilation. Severe hypoxia initially increased ventilation, but then induced suppression of ventilation together with inhibition of EEG signals. It could be explained by a reduction of central command from the higher brain to the brainstem respiratory center. This mechanism may underlie the pathophysiology of respiratory arrest in cases loaded with severe acute hypoxia.

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