Wagner C D, Just A, Nafz B, Persson P B
Institut für Physiologie der Humboldt-Universität zu Berlin (Charité), Germany.
Am J Physiol. 1997 Jun;272(6 Pt 2):R2034-9. doi: 10.1152/ajpregu.1997.272.6.R2034.
The aim of this study was to investigate spontaneous variability of arterial blood pressure in conscious foxhounds in the absence of direct sympathetic and parasympathetic influences. Autonomic blockade was achieved by administration of the ganglionic blocking agent hexamethonium (n = 7). In contrast to the control group (n = 7), marked oscillations with a cycle length of 100 s (0.01 Hz) were observed. The relationship of the power densities of the oscillation band (0.01 +/- 0.005 Hz) to the total power increased threefold (0.213 +/- 0.007 vs. 0.057 +/- 0.005; P < 0.01). The 0.01-Hz oscillations typically commenced after some delay. To test whether the absence of the mechanoreceptor afferents was responsible for these fluctuations, we investigated an additional group of foxhounds that were subjected to total baroreceptor and cardiopulmonary receptor denervation (n = 7). Neither in this protocol, nor in a group subjected to denervation and ganglionic blockade (n = 6), did we observe sustained oscillations in this frequency range. Since the oscillations were not seen after combined afferent (mechanoreceptor denervation) and efferent (ganglionic) blockade, central oscillators as a source of the oscillations can be ruled out. A simple model of a circulating pressoric factor may explain the fluctuations, provided that there is a time delay between the stimulus and the release or action of the factor. The findings suggest that a circulating factor accounts for the 0.01-Hz oscillations, which is dependent on intact pathways from the cardiac receptors or baroreceptors to the central nervous system. This hypothesis is put forward since cardiopulmonary and baroreceptor denervation blocked the oscillations seen after ganglionic blockade.
本研究的目的是在无直接交感神经和副交感神经影响的情况下,研究清醒猎狐犬动脉血压的自发变异性。通过给予神经节阻断剂六甲铵(n = 7)实现自主神经阻断。与对照组(n = 7)相比,观察到周期长度为100秒(0.01赫兹)的明显振荡。振荡带(0.01±0.005赫兹)的功率密度与总功率的关系增加了两倍(0.213±0.007对0.057±0.005;P < 0.01)。0.01赫兹的振荡通常在延迟一段时间后开始。为了测试机械感受器传入神经的缺失是否是这些波动的原因,我们研究了另一组接受完全压力感受器和心肺感受器去神经支配的猎狐犬(n = 7)。在该方案中,以及在接受去神经支配和神经节阻断的组(n = 6)中,我们均未在该频率范围内观察到持续振荡。由于在传入(机械感受器去神经支配)和传出(神经节)联合阻断后未观察到振荡,因此可以排除中枢振荡器作为振荡源。一个简单的循环压力因子模型可以解释这些波动,前提是在刺激与该因子的释放或作用之间存在时间延迟。研究结果表明,一种循环因子导致了0.01赫兹的振荡,这依赖于从心脏感受器或压力感受器到中枢神经系统的完整通路。提出这一假设是因为心肺和压力感受器去神经支配阻断了神经节阻断后出现的振荡。