Moraes Davi J A, Bonagamba Leni G H, Costa Kauê M, Costa-Silva João H, Zoccal Daniel B, Machado Benedito H
Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900, Ribeirão Preto, SP, Brazil.
J Physiol. 2014 May 1;592(9):2013-33. doi: 10.1113/jphysiol.2013.262212. Epub 2014 Mar 10.
Individuals experiencing sustained hypoxia (SH) exhibit adjustments in the respiratory and autonomic functions by neural mechanisms not yet elucidated. In the present study we evaluated the central mechanisms underpinning the SH-induced changes in the respiratory pattern and their impact on the sympathetic outflow. Using a decerebrated arterially perfused in situ preparation, we verified that juvenile rats exposed to SH (10% O2) for 24 h presented an active expiratory pattern, with increased abdominal, hypoglossal and vagal activities during late-expiration (late-E). SH also enhanced the activity of augmenting-expiratory neurones and depressed the activity of post-inspiratory neurones of the Bötzinger complex (BötC) by mechanisms not related to changes in their intrinsic electrophysiological properties. SH rats exhibited high thoracic sympathetic activity and arterial pressure levels associated with an augmented firing frequency of pre-sympathetic neurones of the rostral ventrolateral medulla (RVLM) during the late-E phase. The antagonism of ionotropic glutamatergic receptors in the BötC/RVLM abolished the late-E bursts in expiratory and sympathetic outputs of SH rats, indicating that glutamatergic inputs to the BötC/RVLM are essential for the changes in the expiratory and sympathetic coupling observed in SH rats. We also observed that the usually silent late-E neurones of the retrotrapezoid nucleus/parafacial respiratory group became active in SH rats, suggesting that this neuronal population may provide the excitatory drive essential to the emergence of active expiration and sympathetic overactivity. We conclude that short-term SH induces the activation of medullary expiratory neurones, which affects the pattern of expiratory motor activity and its coupling with sympathetic activity.
经历持续性缺氧（SH）的个体通过尚未阐明的神经机制对呼吸和自主功能进行调节。在本研究中，我们评估了支撑SH诱导的呼吸模式变化的中枢机制及其对交感神经输出的影响。使用去大脑原位动脉灌注制备，我们证实暴露于SH（10%氧气）24小时的幼年大鼠呈现主动呼气模式，在呼气后期（late-E）腹部、舌下和迷走神经活动增加。SH还通过与其内在电生理特性变化无关的机制增强了增强呼气神经元的活动，并抑制了Bötzinger复合体（BötC）吸气后神经元的活动。SH大鼠在late-E期表现出高胸段交感神经活动和动脉压水平，这与延髓头端腹外侧区（RVLM）交感神经节前神经元的放电频率增加有关。BötC/RVLM中离子型谷氨酸能受体的拮抗作用消除了SH大鼠呼气和交感神经输出中的late-E爆发，表明向BötC/RVLM的谷氨酸能输入对于SH大鼠中观察到的呼气和交感神经耦合变化至关重要。我们还观察到，通常沉默的梯形核/面神经旁呼吸组的late-E神经元在SH大鼠中变得活跃，这表明该神经元群体可能为主动呼气和交感神经过度活动的出现提供必要的兴奋性驱动。我们得出结论，短期SH诱导延髓呼气神经元的激活，这影响呼气运动活动模式及其与交感神经活动的耦合。
