Department of Pediatrics, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756, United States.
Respir Physiol Neurobiol. 2013 Jan 1;185(1):132-43. doi: 10.1016/j.resp.2012.06.005. Epub 2012 Jun 8.
Arousal from sleep is a major defense mechanism in infants against hypoxia and/or hypercapnia. Arousal failure may be an important contributor to SIDS. Areas of the brainstem that have been found to be abnormal in a majority of SIDS infants are involved in the arousal process. Arousal is sleep state dependent, being depressed during AS in most mammals, but depressed during QS in human infants. Repeated exposure to hypoxia causes a progressive blunting of arousal that may involve medullary raphe GABAergic mechanisms. Whereas CB chemoreceptors contribute heavily to arousal in response to hypoxia, serotonergic central chemoreceptors have been implicated in the arousal response to CO(2). Pulmonary or chest wall mechanoreceptors also contribute to arousal in proportion to the ventilatory response and decreases in their input may contribute to depressed arousal during AS. Little is known about specific arousal pathways beyond the NTS. Whether CB chemoreceptor stimulation directly stimulates arousal centers or whether this is done indirectly through respiratory networks remains unknown. This review will focus on arousal in response to hypoxia and CO(2) in the fetus and newborn and will outline what we know (and do not know) about the involvement of the carotid body in this process.
从睡眠中觉醒是婴儿对抗缺氧和/或高碳酸血症的主要防御机制。觉醒失败可能是 SIDS 的一个重要原因。在大多数 SIDS 婴儿中发现异常的脑干区域参与觉醒过程。觉醒是睡眠状态依赖性的，在大多数哺乳动物的 AS 期间被抑制，但在人类婴儿的 QS 期间被抑制。反复暴露于缺氧会导致觉醒逐渐迟钝，这可能涉及延髓中缝核 GABA 能机制。虽然 CB 化学感受器在缺氧反应中对觉醒有很大贡献，但 5-羟色胺能中枢化学感受器也与 CO2 反应中的觉醒反应有关。肺或胸壁机械感受器也根据通气反应来促进觉醒，其输入的减少可能导致 AS 期间的觉醒抑制。关于 NTS 以外的特定觉醒途径知之甚少。CB 化学感受器刺激是否直接刺激觉醒中枢，或者是否通过呼吸网络间接刺激，目前尚不清楚。这篇综述将重点介绍胎儿和新生儿对缺氧和 CO2 的觉醒反应，并概述我们对颈动脉体在这一过程中的参与了解（和不了解）。
