Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system.
Physiological and pathophysiological interactions between the respiratory central pattern generator and the sympathetic nervous system.
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DOI：
10.1016/b978-0-444-63488-7.00001-x
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发表时间：
2014
影响因子：
--
通讯作者：
Rybak IA
中科院分区：
文献类型：
--
作者：
Molkov YI;Zoccal DB;Baekey DM;Abdala AP;Machado BH;Dick TE;Paton JF;Rybak IA
在交感神经活动（SNA）中看到的呼吸调制意味着呼吸和交感神经网络相互作用。在慢性间歇性缺氧（CIH）引起的高血压期间，SNA显示出增强的呼吸调节，反映了网络之间加强的相互作用。在本章中，我们回顾了一系列的实验和建模研究，有助于阐明可能的机制交感神经呼吸耦合。我们的结论是，这种耦合显着有助于交感神经压力感受器反射和增强交感神经活动后，暴露于CIH。这一结论基于以下调查结果。(1)压力感受器激活通过BötC中吸气后神经元的短暂激活导致呼吸模式的扰动。相同的BötC神经元参与SNA的呼吸调节，因此为交感压力感受器反射提供了额外的通路。(2)在高碳酸血症下，腹运动神经（AbN）的阶段性激活伴随SNA中的同步放电，这是由于在后斜方核（RTN）中的这种节律性活动的共同来源。CIH调节增加了RTN中中枢化学感受器的CO2敏感性，这导致在正常碳酸血症条件下出现AbN和SNA放电，类似于在幼稚动物中高碳酸血症期间观察到的那些。因此，交感神经-交感神经相互作用在定义交感神经输出中起着重要作用，并且在某些生理或病理生理条件下对交感神经活动和高血压有显著贡献，并且所提出的理论框架可能有助于理解在各种疾病状态下交感神经活动的故障控制。
Respiratory modulation seen in the sympathetic nerve activity (SNA) implies that the respiratory and sympathetic networks interact. During hypertension elicited by chronic intermittent hypoxia (CIH), the SNA displays an enhanced respiratory modulation reflecting strengthened interactions between the networks. In this chapter, we review a series of experimental and modeling studies that help elucidate possible mechanisms of sympatho-respiratory coupling. We conclude that this coupling significantly contributes to both the sympathetic baroreflex and the augmented sympathetic activity after exposure to CIH. This conclusion is based on the following findings. (1) Baroreceptor activation results in perturbation of the respiratory pattern via transient activation of postinspiratory neurons in the Bötzinger complex (BötC). The same BötC neurons are involved in the respiratory modulation of SNA, and hence provide an additional pathway for the sympathetic baroreflex. (2) Under hypercapnia, phasic activation of abdominal motor nerves (AbN) is accompanied by synchronous discharges in SNA due to the common source of this rhythmic activity in the retrotrapezoid nucleus (RTN). CIH conditioning increases the CO2 sensitivity of central chemoreceptors in the RTN which results in the emergence of AbN and SNA discharges under normocapnic conditions similar to those observed during hypercapnia in naïve animals. Thus, respiratory–sympathetic interactions play an important role in defining sympathetic output and significantly contribute to the sympathetic activity and hypertension under certain physiological or pathophysiological conditions, and the theoretical framework presented may be instrumental in understanding of malfunctioning control of sympathetic activity in a variety of disease states.