Sympathetic activation by the central chemoreceptor 'reflex': new evidence that RVLM vasomotor neurons are involved...but are they enough?
Sympathetic activation by the central chemoreceptor 'reflex': new evidence that RVLM vasomotor neurons are involved...but are they enough?
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中枢化学感受器“反射”激活交感神经：新证据表明 RVLM 血管运动神经元参与其中……但它们足够了吗？
DOI：
10.1113/jphysiol.2006.119677
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Toney,GlennM
中科院分区：
文献类型：
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作者：
Toney,GlennM
化学感受神经元在中枢神经系统中的存在早在40多年前就被发现了（Mitchell et al. 1963）。随后，研究表明，即使溶解二氧化碳（CO2）的少量增加（即高碳酸血症）也会使脑脊液（CSF）酸化，从而激活化学感受器神经元，从而刺激“呼吸的驱动力”（Feldman et al. 2003; Nattie & Li, 2006）。早期（Mitchell et al. 1963）和最近（Mulkey et al. 2004）的研究表明，呼吸刺激是否完全/主要由髓质腹侧表面的神经元介导，或者是脑干化学受体神经元网络的一种突现特性（Smith et al. 2006），这仍然是一个充满活力的对话的来源（Nattie & Li, 2006）。在这一期的《生理学杂志》上，Moreira等人（2006）将注意力转向了对碳酸过高反应的另一个重要组成部分，即增加的交感神经放电（SND）。虽然与高碳酸血症对呼吸的影响相比，研究较少，但当吸入气体变得高碳酸血症或酸碱平衡被破坏时，动脉/脑脊液二氧化碳升高引起的交感神经激活具有重要的体内平衡功能，可以在呼吸抑制期间维持适当的脑和全身血流分布（Dean et al. 1990; Feldman et al.）。
The existence of chemoreceptive neurons in the central nervous system was discovered more than 40 years ago (Mitchell et al. 1963). Subsequently, studies have demonstrated that cerebrospinal fluid (CSF) acidification by even a small increase in dissolved carbon dioxide (CO2)(ie hypercapnoea) activates chemoreceptor neurons and thereby stimulates the ‘drive to breathe’(Feldman et al. 2003; Nattie & Li, 2006). Whether respiratory stimulation is mediated exclusively/predominantly by neurons within the ventral surface of the medulla as suggested by early (Mitchell et al. 1963) and more recent (Mulkey et al. 2004) studies, or is an emergent property of a brainstem network of chemoreceptor neurons (Smith et al. 2006) continues to be a source of spirited dialog (Nattie & Li, 2006). In this issue of The Journal of Physiology, Moreira et al.(2006) shift attention toward another important component of the response to hypercapnoea, namely increased sympathetic nerve discharge (SND). Though less well studied than respiratory effects of hypercapnoea, sympathetic activation by elevated arterial/CSF CO2 has important homeostatic functions that maintain appropriate cerebral and systemic blood flow distribution during respiratory depression, when inspired gases become hypercapnic, or when acid–base balance is disrupted (Dean et al. 1990; Feldman et al.