Richardson C A
Cardiovascular Research Institute, School of Medicine, University of California, San Francisco 94143-0542.
J Appl Physiol (1985). 1988 Apr;64(4):1709-20. doi: 10.1152/jappl.1988.64.4.1709.
To investigate the effect of lung inflations on the high-frequency synchrony (70-122 Hz) observed in the inspiratory activity of respiratory motor nerves of decerebrate cats, I applied a step increase in lung inflation pressure at fixed delays into the inspiratory phase and computed power spectra of phrenic neurograms before and during inflation. In 25 decerebrate paralyzed cats the frequency of the high spectral peak was 92.3 +/- 11.1 Hz before and 105.3 +/- 12.1 Hz during the step in inflation pressure, shifting upward by 13.0 +/- 6.0 Hz. For 8 of the 25 cats, the recurrent laryngeal and phrenic neurograms were recorded simultaneously. The high spectral peak was present during inspiration in the recurrent laryngeal power spectra and coherent with the high peak in the phrenic power spectra. In response to lung inflation, the high peak disappeared from the power spectra of the recurrent laryngeal nerve as the inspiratory activity was inhibited; a shift upward in frequency was not detectable. Comparing inspiratory times (TI, based on the phrenic neurograms) for breaths with no lung inflations to those for breaths with lung inflations, I found that lung inflations early in inspiration caused a decrease in TI, lung inflations at intermediates times had no effect on TI, and lung inflations late in inspiration caused an increase in TI. Despite lung inflation decreasing, not affecting, or increasing inspiratory duration and amplitude of the phrenic neurogram, lung inflation always caused a shift upward in the high-frequency peak of the phrenic power density. The fact that lung inflation, a powerful respiratory stimulus, affected the frequency of the high peak in a consistent manner suggests that the high-frequency synchrony is an important and robust feature of the central respiratory pattern generator.
为了研究肺膨胀对去大脑猫呼吸运动神经吸气活动中观察到的高频同步(70 - 122赫兹)的影响,我在吸气相的固定延迟时刻施加肺膨胀压力的阶跃增加,并计算膨胀前和膨胀期间膈神经图的功率谱。在25只去大脑麻痹的猫中,膨胀压力阶跃前高频谱峰的频率为92.3±11.1赫兹,膨胀期间为105.3±12.1赫兹,向上移动了13.0±6.0赫兹。在这25只猫中的8只中,同时记录了喉返神经和膈神经图。在喉返神经功率谱的吸气期间存在高频谱峰,并且与膈神经功率谱中的高频峰相干。响应肺膨胀,随着吸气活动受到抑制,高频峰从喉返神经的功率谱中消失;未检测到频率向上偏移。比较无肺膨胀呼吸和有肺膨胀呼吸的吸气时间(基于膈神经图),我发现吸气早期的肺膨胀导致吸气时间减少,中期的肺膨胀对吸气时间没有影响,而吸气晚期的肺膨胀导致吸气时间增加。尽管肺膨胀会减少、不影响或增加膈神经图的吸气持续时间和幅度,但肺膨胀总是会导致膈神经功率密度的高频峰向上移动。强大的呼吸刺激肺膨胀以一致的方式影响高频峰的频率这一事实表明,高频同步是中枢呼吸模式发生器的一个重要且稳健的特征。