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新生儿缺氧时双相呼吸模式的中枢起源

Central origin of biphasic breathing pattern during hypoxia in newborns.

作者信息

Lawson E E, Long W A

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1983 Aug;55(2):483-8. doi: 10.1152/jappl.1983.55.2.483.

DOI:10.1152/jappl.1983.55.2.483
PMID:6413465
Abstract

The ventilatory response to moderate hypoxia of both animal and human newborns differs significantly from that of adults. The newborn response is characterized by transient hyperpnea followed by return of ventilation toward or below the control level and even apnea. To determine whether central respiratory control mechanisms are affected by hypoxia in newborns, we used an anesthetized, paralyzed, mechanically ventilated piglet model in which the vagus nerves were cut. Respiratory activity was determined by measuring electrical activity of a cut phrenic nerve. During a 6-min continuous exposure to 15% O2 as the inspired gas, 11 piglets increased their respiratory output to 181 +/- 38% of the control value within 2.5 min. However, by the 6th min the average respiratory output had declined to 104 +/- 25% of the control. During the exposure to hypoxia, the servo-controlled ventilator frequency (an index of CO2 flux to the lungs) was persistently greater than control (28.0 +/- 1.0 vs. 30.5 +/- 1.4 cycles/min; P less than 0.01). These data indicate that the newborn's characteristic breathing response to hypoxia is due to failure of central neural respiratory control mechanisms. Paralysis, constant end-tidal PCO2, and increased ventilator rate during hypoxia exclude changes in pulmonary mechanics or decreased metabolic rate as explanations of the paradoxical decline in respiratory output.

摘要

动物和人类新生儿对中度缺氧的通气反应与成年人有显著差异。新生儿的反应特点是短暂的呼吸急促,随后通气恢复到或低于控制水平,甚至出现呼吸暂停。为了确定新生儿的中枢呼吸控制机制是否受缺氧影响,我们使用了一种麻醉、麻痹、机械通气的仔猪模型,该模型切断了迷走神经。通过测量切断的膈神经的电活动来确定呼吸活动。在将吸入气体持续暴露于15%氧气6分钟的过程中,11只仔猪在2.5分钟内将其呼吸输出增加到对照值的181±38%。然而,到第6分钟时,平均呼吸输出已降至对照值的104±25%。在缺氧暴露期间,伺服控制的通气频率(二氧化碳向肺部通量的指标)持续高于对照值(28.0±1.0对30.5±1.4次/分钟;P<0.01)。这些数据表明,新生儿对缺氧的特征性呼吸反应是由于中枢神经呼吸控制机制失灵。麻痹、恒定的呼气末二氧化碳分压以及缺氧期间通气频率增加排除了肺力学变化或代谢率降低作为呼吸输出矛盾性下降的解释。

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