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麻醉大鼠迷走神经(喉上神经)、舌下神经和膈神经之间呼吸神经活动的差异。

Differences in respiratory neural activities between vagal (superior laryngeal), hypoglossal, and phrenic nerves in the anesthetized rat.

作者信息

Fukuda Y, Honda Y

出版信息

Jpn J Physiol. 1982;32(3):387-98. doi: 10.2170/jjphysiol.32.387.

Abstract

Respiratory neural activities were recorded from the efferent vagal (superior laryngeal Xsl)), hypoglossal (XII), and phrenic nerves in spontaneously breathing rats anesthetized with halothane. The onset of inspiratory discharges in the cranial nerves was slightly earlier (5-60 msec) but more gradual than that of phrenic bursts. When the anesthesia was deepened by increasing the concentration of halothane or by injection of pentobarbital, inspiratory discharges in the three nerves were well maintained although there was a progressive decrease in respiratory frequency and a prolongation of the delay from the start of Xsl or XII inspiratory activities to the onset of phrenic bursts. Inhalation of CO2 increased respiratory frequency and augmented the peak phrenic activity whereas the peak inspiratory activities in the cranial nerves remained unchanged under elevated end-tidal PCO2. Both in deeper anesthesia and in hypercapnia, changes in respiratory frequency were due mainly to alterations in the duration of expiration. The results indicated that the rat, 1) overall inspiratory activities in various nerves innervating the diaphragm and accessory respiratory muscles in the upper airway are quite resistant to depressing actions of halothane or halothane-pentobarbital anesthesia, although the mechanism controlling respiratory frequency is strongly affected, and 2) excitatory signals elicited by an elevated PCO2 via respiratory chemosensors preferentially augment inspiratory activities in the phrenic nerve. Factors influencing the temporal difference in the onset of inspiratory activities in the cranial and phrenic nerves are discussed.

摘要

在使用氟烷麻醉的自主呼吸大鼠中,记录了迷走神经传出支(喉上神经Xsl)、舌下神经(XII)和膈神经的呼吸神经活动。颅神经吸气放电的起始略早(5 - 60毫秒),但比膈神经爆发更缓慢。当通过增加氟烷浓度或注射戊巴比妥加深麻醉时,尽管呼吸频率逐渐降低,且从Xsl或XII吸气活动开始到膈神经爆发开始的延迟延长,但三条神经的吸气放电仍能良好维持。吸入二氧化碳会增加呼吸频率并增强膈神经的峰值活动,而在呼气末PCO2升高的情况下,颅神经的吸气峰值活动保持不变。在深度麻醉和高碳酸血症时,呼吸频率的变化主要是由于呼气持续时间的改变。结果表明,大鼠,1)支配膈肌和上呼吸道辅助呼吸肌的各种神经的总体吸气活动对氟烷或氟烷 - 戊巴比妥麻醉的抑制作用相当耐受,尽管控制呼吸频率的机制受到强烈影响,并且2)通过呼吸化学感受器由升高的PCO2引发的兴奋性信号优先增强膈神经的吸气活动。讨论了影响颅神经和膈神经吸气活动起始时间差异的因素。

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