Gebber Gerard L, Das Mahasweta, Barman Susan M
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, 48824-1317, USA.
Brain Res. 2005 Jun 7;1046(1-2):216-23. doi: 10.1016/j.brainres.2005.04.009.
In urethane-anesthetized, paralyzed, and artificially ventilated cats, we observed an unusual form of "phase walk" of the cardiac-related burst of inferior cardiac postganglionic sympathetic nerve discharge (SND) relative to the systolic phase of the arterial pulse (AP) and thus pulse-synchronous baroreceptor nerve activity. Unlike classic phase walk ascribable to weakened coupling (desynchronization) of two oscillators, AP-SND phase walk was characterized by epochs of progressive, bidirectional changes in the angle of strong coupling (AP-SND coherence values, >0.9) of these signals that recurred on the time scale of the respiratory cycle and whose range was approximately one third of the period of the heart beat. AP-SND phase walk was linked to two respiratory variables (central respiratory drive and vagal lung inflation afferent activity) as demonstrated by the following observations. First, in five normocapnic cats (end-tidal CO(2), 4.3 +/- 0.2%) with intact vagus nerves and three vagotomized cats, AP-SND phase walk was characterized by a progressive heart-beat-to-heart-beat decrease in the lag of SND relative to the AP during the inspiratory phase of phrenic nerve activity and an increase in the lag during the expiratory phase. Second, in three cats with intact vagus nerves that were hyperventilated (end tidal CO(2), 1.6 +/- 0.4%) to phrenic nerve quiescence, the lag of the cardiac-related burst of SND relative to the AP increased during lung inflation and decreased during lung deflation. Additional experimentation revealed that AP-SND phase walk is attributable to respiratory-induced changes in the frequency of the centrally generated sympathetic nerve rhythm rather than heart rate. Moreover, the data demonstrate that the frequency and amplitude of the sympathetic oscillation are independently controlled by the above mentioned respiratory parameters.
在氨基甲酸乙酯麻醉、麻痹并进行人工通气的猫身上,我们观察到心脏相关的下心脏节后交感神经放电(SND)爆发相对于动脉脉搏(AP)的收缩期以及脉搏同步压力感受器神经活动呈现出一种不寻常的“相位游走”形式。与可归因于两个振荡器耦合减弱(去同步化)的经典相位游走不同,AP - SND相位游走的特征是这些信号的强耦合角度(AP - SND相干值,>0.9)出现渐进性、双向变化的时期,这些变化在呼吸周期的时间尺度上反复出现,其范围约为心跳周期的三分之一。如下观察结果所示,AP - SND相位游走与两个呼吸变量(中枢呼吸驱动和迷走神经肺膨胀传入活动)有关。首先,在五只迷走神经完整的正常碳酸血症猫(呼气末二氧化碳,4.3±0.2%)和三只迷走神经切断的猫中,AP - SND相位游走的特征是在膈神经活动的吸气期,SND相对于AP的延迟逐心跳地逐渐减小,而在呼气期延迟增加。其次,在三只迷走神经完整的猫中,使其过度通气(呼气末二氧化碳,1.6±0.4%)至膈神经静止,与AP相关的SND爆发延迟在肺充气时增加,在肺放气时减少。进一步的实验表明,AP - SND相位游走归因于呼吸引起的中枢产生的交感神经节律频率变化,而非心率变化。此外,数据表明交感神经振荡的频率和幅度由上述呼吸参数独立控制。