Respiratory neuronal activity during apnea and other breathing patterns induced by laryngeal stimulation.
Respiratory neuronal activity during apnea and other breathing patterns induced by laryngeal stimulation.
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呼吸暂停和喉部刺激引起的其他呼吸模式期间的呼吸神经元活动。
DOI：
10.1152/jappl.1991.70.6.2742
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Rudesill,RC
中科院分区：
文献类型：
--
作者：
Lawson,EE;Richter,DW;Czyzyk-Krzeska,MF;Bischoff,A;Rudesill,RC
呼吸循环通过三个不同的阶段（吸气，吸气后和呼气），每个阶段都有相应的髓细胞，在一个阶段被兴奋，在其他两个阶段被抑制。已知喉刺激可诱导新生动物呼吸暂停，但这种作用的细胞机制尚不清楚。腹侧呼吸组神经元的细胞内记录完成在完整的麻醉，麻痹，和机械通气的小猪。通过向喉部吹入氨饱和空气、烟雾或水诱导呼吸暂停。喉吹气诱导膈神经呼吸暂停，吸气后神经元的刺激，和稳定的吸气和呼气细胞的膜电位与吸气后抑制一致。通常，每种神经元类型的膜电位在第一次恢复呼吸开始之前循环通过呼气水平。还观察到呼吸暂停反应的变体，可能反映了吸气反射或嗅、打喷嚏、咳嗽和吞咽。这些后者的模式表现出吸气和吸气后没有明显的干预阶段II呼气相之间的振荡。然而，第二阶段的呼气活动总是在这样的模式后的第一个斜坡吸气开始之前。这些研究结果表明，吸气后机制的激活导致呼吸模式的深刻变化，第二阶段呼气重要地调节斜坡吸气活动的恢复。后一种效应的机制可能是抑制早期吸气神经元，随后出现抑制后反弹。
Respiration cycles through three distinct phases (inspiration, postinspiration, and expiration) each having corresponding medullary cells that are excited during one phase and inhibited during the other two. Laryngeal stimulation is known to induce apnea in newborn animals, but the cellular mechanisms underlying this effect are not known. Intracellular recording of ventral respiratory group neurons was accomplished in intact anesthetized, paralyzed, and mechanically ventilated piglets. Apnea was induced by insufflation of the larynx with ammonia-saturated air, smoke, or water. Laryngeal insufflation induced phrenic nerve apnea, stimulation of postinspiratory neurons, and stable membrane potentials in inspiratory and expiratory cells consistent with postinspiratory inhibition. Usually the membrane potential of each neuronal type cycled through an expiratory level before onset of the first recovery breath. Variants of the apnea response, probably reflecting the aspiration reflex or sniffing, sneezing, coughing, and swallowing, were also observed. These latter patterns showed oscillation between inspiration and postinspiration without an apparent intervening stage II expiratory phase. However, stage II expiratory activity always preceded onset of the first ramp inspiration after such a pattern. These findings suggest that activation of postinspiratory mechanisms causes profound alterations in the respiratory pattern and that stage II expiration importantly modulates recovery of ramp inspiratory activity. The mechanism of this latter effect may be inhibition of early inspiratory neurons with consequent postinhibitory rebound.