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研究生: 郭昶志
Kuo, Chung-Chih
論文名稱: 貓延腦吻端腹外側對喉返神經呼吸活動的影響
Effect of the rostral ventrolateral medulla on respiratory-
指導教授: 黃基礎
Hwang, Ji-Chuu
學位類別: 碩士
Master
系所名稱: 生命科學系
Department of Life Science
畢業學年度: 84
語文別: 中文
論文頁數: 62
中文關鍵詞: 延腦吻端腹外側喉返神經上呼吸道膈神經
英文關鍵詞: rostral ventrolateral medulla, recurrent laryngeal nerve, upper airway, phrenic nerve
論文種類: 學術論文
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  • 本研究之目的在探討貓延腦吻端腹外側如何影響喉返神經的呼吸活
    動。選用去 大腦貓,切斷兩側迷走神經,以肌肉麻痺劑麻痺後,由人工
    呼吸機維持其生命,在高 氧二氧化碳濃度正常狀態下,以電刺激(12.5
    to 50 mA, 80 Hz, 0.5 ms)或化學刺 激(50 mM, 30-60 nl)方式興奮
    rVLM,觀察膈神經及喉返神經呼吸活動的變化。 在呼氣末二氧化碳
    濃度為 0.04 的狀態下,對 19 隻動物之延腦吻端腹外側作 12.5、25 和
    50μA 電刺激,膈神經吸氣活動高度分別降低為刺激前的 93.3%、74.9
    %(p<0.01)和 50.3%(p<0.01),喉返神經吸氣活動高度分別降低為
    刺激前的 85.1%(p<0.05)、71.6%(p<0.01)和 54.7%(p<0.01),
    而喉返神經呼氣活動高度分別降低為刺激前的 84.4%(p<0.05)、75.5
    %(p<0.01)和 63.6%(p<0.01);以麩胺酸鈉 (glutamate 50 mM,
    體積 30-60 nl)刺激 13 隻動物之延腦吻端腹外側,膈神經吸氣活動高
    度降低為刺激前的 65.4%(p<0.01),喉返神經吸氣活動高度降低為刺
    激前的 75.2%(p<0.01),喉返神經呼氣活動高度降低為刺激前的
    53.3%(p<0.01)。提高呼氣末二氧化碳濃度可降低 rVLM 對喉返神經呼
    吸活動的抑制作用。在 FETCO2=0.06,25 μA 電刺激 rVLM 後,膈神經
    活動為刺激前的 83.4%(p<0.05),喉返神經吸氣活動為刺激前的
    78.5%(p<0.01),喉返神經呼氣活動為刺激前的 62.8%(p<0.01);50
    μA 電 刺激 rVLM後,膈神經活動為刺激前的 56.3%(p<0.01),喉返神
    經吸氣活動為刺激前的53.5%(p< 0.01),喉返神經呼氣活動為刺激前的
    43.9%(p<0.01)。當FETCO2=0.09,25 μA 電刺激 rVLM 後,膈神經活
    動為刺激前的 89.5%(p<0.05),喉返神經吸氣活動為刺激前的 87.2
    %,喉返神經呼氣活動為刺激前的 77.4%(p<0.05);50 μA 電刺激
    rVLM 後,膈神經活動為刺激前的 65.5%(p<0.01),喉返神經吸氣活動
    為刺激前的 59.2%(p<0.01),喉返神經呼氣活動為刺激前的 44.3%(
    p<0.01)。 由以上之結果可知,延腦吻端腹外
    側對喉返神經呼吸活動具有抑制作用,提高二氧化碳濃度可降低此種抑制
    作用,推論延腦吻端腹外側在上呼吸道的阻力管制中可能扮演重要的角色

    The purpose of the present study was to evaluate the effect
    of the rostralventrolateral medulla (rVLM) on respiratory-
    related activity of the recurrentlaryngeal nerve (RLN). The
    animal was decerebrated, vagatomized paralyzed and ventilated
    artificially. Activities of the phrenic (PNA) and recurrent
    laryngeal nerve (RLNA) were monitored at normocapnia or
    hypercapnia both in hyperoxia. The rVLM was activated by
    electrical current (12.5 to 50 mA, 80 Hz, 0.5 ms) or glutamate
    (50 mM, 30-60 nl). Changes of PNA and RLNA are observed. In
    response to current of 12.5, 25 and 50 mA delivered to the rVLM,
    PNA were reduced to 93.3%, 74.9% (p<0.01) and 50.3% (p<0.01) of
    control respectively. Meanwhile, inspiratory RLNA (iRLNA) were
    reduced to 85.1% (p<0.05), 71.6% (p<0.01) and 54.7% (p<0.01) of
    control and expiratory RLNA (eRLNA) are reduced to 84.4%
    (p<0.05), 75.5% (p<0.01) and 63.6% (p<0.01) of control. With
    glutamate microinjection into the rVLMs, PNA, inspiratory and
    expiratory RLNA were decreased to 65.4% (p<0.01), 75.2% (p<0.01)
    and 53.3% (p<0.01) of control. This inhibition of the rVLM upon
    PNA and RLNA was attenuated by high level of FETCO2. Hence, at
    mild hypercapnia ( FETCO2=0.06), 25 mA delivery to the rVLM
    produced a decrease of PNA to 83.4% (p<0.05), iRLNA to 78.5%
    (p<0.01) and eRLNA to 62.8% of control. 50 mA delivery to the
    rVLM produced a decrease of PNA to 56.3% (p<0.01), iRLNA to
    53.5% (p<0.01) and eRLNA to 43.9% (p<0.01) of control. When
    FETCO2 was further raised to 0.09, current of 25 mA excited to
    the rVLM could produce a decrease of PNA to 89.5% (p<0.05),
    iRLNA to 87.2% and eRLNA to 77.4% (p<0.05) of control. 50 mA
    delivery to the rVLM produced a decrease of PNA to 65.5%
    (p<0.01), iRLNA to 59.2% (p<0.01) and eRLNA to 44.3%
    (p<0.01) of control.

    These results suggest that the rVLM may play an important role
    in the modulation mechanism of upper airway resistance.
    The purpose of the present study was to evaluate the effect

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