Connelly C A, Wurster R D
Am J Physiol. 1985 Oct;249(4 Pt 2):R424-31. doi: 10.1152/ajpregu.1985.249.4.R424.
The effect of hyperventilation-induced apnea on the respiratory rhythmicity of sympathetic nerve activity was determined using spectral analysis of sympathetic nerve frequencies. Left phrenic, external intercostal, and inferior cardiac sympathetic nerves were recorded in alpha-chloralose-anesthetized, vagotomized, paralyzed, artificially ventilated cats. The respiratory modulation of sympathetic activity during normoventilation was indicated by spectral peaks of sympathetic activity coinciding with respiratory frequencies determined from the phrenic nerve activity of each cat. The spectral peaks of respiratory-related sympathetic activity disappeared during hyperventilation-induced apnea and then reappeared with the return of phrenic nerve activity when normoventilation was resumed. Although sympathetic activity lost its respiratory modulation during hyperventilation, baroreceptor-mediated bilateral carotid occlusion responses and electrocardiogram (R wave)-triggered computer summation of cardiac related sympathetic activity were unaffected. Hence central respiratory inputs on sympathetic pathways in the central nervous system best explain the origin of respiratory-related sympathetic rhythms. Independent sympathetic rhythms of apparent nonrespiratory origin may be due to artificial ventilator influences, baroreflex-autonomic oscillation loops, or Mayer waves.
通过对交感神经频率进行频谱分析，确定了过度通气诱发的呼吸暂停对交感神经活动呼吸节律性的影响。在α-氯醛糖麻醉、迷走神经切断、麻痹、人工通气的猫身上记录左膈神经、肋间外肌和心脏下交感神经。正常通气期间交感神经活动的呼吸调制通过交感神经活动的频谱峰值来表明，这些峰值与根据每只猫的膈神经活动确定的呼吸频率一致。过度通气诱发的呼吸暂停期间，与呼吸相关的交感神经活动的频谱峰值消失，当恢复正常通气膈神经活动恢复时又重新出现。尽管过度通气期间交感神经活动失去了其呼吸调制，但压力感受器介导的双侧颈动脉闭塞反应以及心电图（R波）触发的心脏相关交感神经活动的计算机总和未受影响。因此，中枢神经系统中交感神经通路上的中枢呼吸输入最能解释与呼吸相关的交感神经节律的起源。明显非呼吸起源的独立交感神经节律可能是由于人工呼吸机影响、压力反射-自主振荡环或迈尔氏波所致。
