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刺激喉上神经导致幼猴出现长时间呼吸暂停。

Prolonged apnea in infant monkeys resulting from stimulation of superior laryngeal nerve.

作者信息

Sutton D, Taylor E M, Lindeman R C

出版信息

Pediatrics. 1978 Apr;61(4):519-27.

PMID:96414
Abstract

We measured characteristics of apnea resulting from electrical stimulation of the superior laryngeal nerve (SLN) in 28 anesthetized infant monkeys ranging from a gestational age of 141 days to 49 days postterm and in four adult monkeys. Progressive reduction in ventilation accompanied weak suprathreshold SLN stimulation. Poststimulus apnea followed stronger stimulation. Apnea duration was directly proportional to stimulus duration, provided that stimulus intensity was at least 1.5 X threshold. Poststimulus apnea periods were briefer in older infants and did not occur in adults. Pao2 measurements in four animals showed that lower values were associated with the longer poststimulus apnea episodes. Upper airway resistance measurements obtained from a subglottal cannula revealed that glottal closure was transiently associated with the onset of SLN stimulation, but the degree of closure diminished during the course of stimulation and was not present during the subsequent period of apnea. The parameters of SLN stimulation determine specific changes in cardiovascular functions independently of their respiratory effects. The results suggest that a brief afferent input from the SLN may have prolonged effects on respiratory regulation in infants. These persisting effects may be an important consideration in sudden infant death syndrome mechanisms.

摘要

我们在28只麻醉的幼猴(胎龄从141天到足月后49天)和4只成年猴中测量了由喉上神经(SLN)电刺激引起的呼吸暂停特征。阈上SLN弱刺激时,通气逐渐减少。较强刺激后出现刺激后呼吸暂停。只要刺激强度至少为阈值的1.5倍,呼吸暂停持续时间与刺激持续时间成正比。刺激后呼吸暂停期在较大婴儿中较短,在成年猴中不出现。对4只动物的动脉血氧分压测量显示,较低值与较长的刺激后呼吸暂停发作相关。从声门下插管获得的上呼吸道阻力测量结果显示,声门关闭与SLN刺激开始短暂相关,但在刺激过程中关闭程度减小,在随后的呼吸暂停期不存在。SLN刺激参数决定心血管功能的特定变化,与其呼吸效应无关。结果表明,来自SLN的短暂传入输入可能对婴儿的呼吸调节有延长作用。这些持续效应可能是婴儿猝死综合征机制中的一个重要考虑因素。

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