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麻醉大鼠呼吸神经调节的缺氧抑制

Hypoxic inhibition of respiratory neural regulation in anesthetized rats.

作者信息

Fukuda Y

机构信息

Department of Physiology II, School of Medicine, Chiba University, Japan.

出版信息

Jpn J Physiol. 1991;41(6):893-906. doi: 10.2170/jjphysiol.41.893.

DOI:10.2170/jjphysiol.41.893
PMID:1806672
Abstract

To determine the neural mechanism of hypoxic respiratory inhibition, discharge patterns of efferent phrenic (Phr), vagal superior laryngeal (Xsl), and vagal pharyngeal (Xphar) nerves were analyzed during systemic hypoxia in the urethane-anesthetized, vagotomized and artificially ventilated rat. In the carotid sinus nerve (CSN) intact rat, moderate hypoxia (end-tidal Po2, 40-50 mmHg) caused an initial increase in respiratory activity which was followed by inhibition due to reduction in respiratory frequency (f). The decrease in f was associated with prolongation of decremental Xphar expiratory (E) activity and retardation of the onset of inspiratory (I) activity. Integrated peak Phr or Xs1 I and Xphar E activities remained augmented during respiratory inhibition. After bilateral CSN section, moderate hypoxia produced an extreme reduction in f due to delayed onset of I activity and a strong reduction in the Xphar E activity. Phr and Xs1 I activities were little affected, and changes in inspiratory time were small. These results suggest that hypoxia centrally inhibits the process of initiating the onset of rhythmic I activity and the activity of decremental Xphar E motoneurons. Carotid chemoreceptor stimulation was inadequate to offset the central inhibitory effect of hypoxia on the onset of I activity.

摘要

为了确定低氧性呼吸抑制的神经机制,在氨基甲酸乙酯麻醉、迷走神经切断并人工通气的大鼠全身低氧期间,分析了传出膈神经(Phr)、迷走神经喉上支(Xsl)和迷走神经咽支(Xphar)的放电模式。在完整颈动脉窦神经(CSN)的大鼠中,中度低氧(呼气末Po2,40 - 50 mmHg)导致呼吸活动最初增加,随后由于呼吸频率(f)降低而受到抑制。f的降低与递减性Xphar呼气(E)活动的延长以及吸气(I)活动起始延迟有关。在呼吸抑制期间,整合的Phr或Xs1 I峰活动以及Xphar E活动仍增强。双侧CSN切断后,中度低氧由于I活动起始延迟导致f极度降低,并且Xphar E活动大幅减少。Phr和Xs1 I活动受影响较小,吸气时间变化不大。这些结果表明,低氧在中枢抑制有节律的I活动起始过程以及递减性Xphar E运动神经元的活动。颈动脉化学感受器刺激不足以抵消低氧对I活动起始的中枢抑制作用。

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