Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA ; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA ; Neuroscience Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA ; Zablocki Veterans Affairs Medical Center, Milwaukee, WI 53226, USA.
Neural Regen Res. 2012 May 15;7(14):1073-9. doi: 10.3969/j.issn.1673-5374.2012.14.005.
Historically, the role of the carotid bodies in ventilatory control has been understated, but the current view suggests that the carotid bodies (1) provide a tonic, facilitory input to the respiratory network, (2) serve as the major site of peripheral O2 chemoreception and minor contributor to CO2/H(+) chemoreception, and (3) are required for ventilatory adaptation to high altitude. Each of these roles has been demonstrated in studies of ventilation in mammals after carotid body denervation. Following carotid body denervation, many of the compromised ventilatory "functions" show a time-dependent recovery plasticity that varies in the degree of recovery and time required for recovery. Respiratory plasticity following carotid body denervation is also dependent on species, with contributions from peripheral and central sites/mechanisms driving the respiratory plasticity. The purpose of this review is to provide a summary of the data pointing to peripheral and central mechanisms of plasticity following carotid body denervation. We speculate that after carotid body denervation there are altered excitatory and/or inhibitory neuromodulator mechanisms that contribute to the initial respiratory depression and the subsequent respiratory plasticity, and further suggest that the continued exploration of central effects of carotid body denervation might provide useful information regarding the capacity of the respiratory network for plasticity following neurologic injury in humans.
从历史上看，颈动脉体在通气控制中的作用被低估了，但目前的观点表明，颈动脉体 (1) 为呼吸网络提供紧张性、易化性输入，(2) 作为外周氧感受器的主要部位，对二氧化碳/氢离子感受器的贡献较小，(3) 是通气适应高原所必需的。这些作用中的每一个都在颈动脉体去神经后的哺乳动物通气研究中得到了证明。在颈动脉体去神经后，许多受损的通气“功能”表现出时间依赖性恢复可塑性，其恢复程度和恢复所需时间各不相同。颈动脉体去神经后的呼吸可塑性也依赖于物种，外周和中枢部位/机制的贡献驱动着呼吸的可塑性。本综述的目的是提供数据的总结，这些数据表明颈动脉体去神经后的外周和中枢可塑性机制。我们推测，在颈动脉体去神经后，兴奋性和/或抑制性神经调质机制发生改变，导致呼吸初始抑制和随后的呼吸可塑性，我们进一步提出，对颈动脉体去神经的中枢作用的进一步探索可能为人类神经系统损伤后呼吸网络的可塑性提供有用信息。
