CONTROL OF BREATHING IN NEWBORNS

尽管新生儿的呼吸调节与 成年人之间存在数量和质量上的差异。 可以 这些发育差异解释了 新生儿易患长时间自发性呼吸暂停。 的 目前的研究是基于这样的假设，即中枢神经机制 在呼吸调节中比传统的 认可. 长期目标是了解 中枢神经机制，使呼吸驱动不稳定。 的 本研究的具体目标是描述 中枢神经机制对呼吸反应缺氧和 呼吸暂停发作后重新开始呼吸。 实验动物 建立了消除负化学效应的模型 通常在通气变化后出现反馈，但允许 通过测量膈神经活动来定量呼吸输出。 两项研究提出了利用这个模型。 一个利用 刺激颈动脉窦神经以刺激缺氧， 利用上级喉神经的刺激来诱导中枢神经系统 呼吸暂停 我们的初步结果表明，刺激神经 激活神经机制， 长时间开车。 此外，这些抑制机制也可能 影响上呼吸道肌肉的神经驱动， 维持气道通畅。 很可能这些抑制机制 是由神经递质介导的。 发射机的不平衡， 刺激和抑制呼吸那些可能在缺氧期间发生。 因此，本研究的第二个目标是确定 缺氧引起的神经递质水平和代谢。 神经化学 脑干生物胺和内啡肽代谢测定 将新生家兔呼吸核分别置于缺氧和对照组 兔子幼崽 中枢兴奋性和抑制性的相互作用 对呼吸中枢的影响可能对 患有呼吸暂停的早产儿以及有呼吸暂停风险的较大婴儿 婴儿猝死综合征和可能患有阻塞性睡眠的成人 呼吸暂停

Though respiratory regulation in newborns has many similarities with adults, quantitative and qualitative differences exist. It is possible that these developmental differences account for the pronounced susceptibility of newborn infants to have prolonged spontaneous apnea. The present studies are based on the hypothesis that central neural mechanisms are more important in respiratory regulation than traditionally recognized. The long-range objective is to develop an understanding of central neural mechanisms which destabilize respiratory drive. The specific objective of this study is to characterize the influence of central neural mechanisms on the respiratory response to hypoxia and on reinitiation of breathing following onset of apnea. An experimental animal model has been developed which eliminates the effect of negative chemical feedback that usually follows a change in ventilation but which allows quantitation of respiratory output by measuring phrenic nerve activity. Two studies are proposed which utilize this model. One utilizes stimulation of th carotid sinus nerve to stimulate hypoxia and the other utilizes stimulation of the superior laryngeal nerve to induce central apnea. Our preliminary results suggest that stimulation of either nerve activates neural mechanisms which serve to inhibit central respiratory drive for a long period. In addition, these inhibition mechanisms may also affect neural drive to upper airway muscles which are important in maintaining airway patency. It is likely that these inhibitory mechanisms are mediated by neurotransmitters. Imbalance of the transmitters that stimulate and those that depress respiration may occur during hypoxia. Therefore, the second objective of this study is to identify changes in neurotransmitter levels and metabolism caused by hypoxia. Neurochemical determinations of biogenic amine and endorphin metabolism in brainstem respiratory nuclei of newborn rabbits will be made in hypoxic and control rabbit pups. The interaction of central excitatory and inhibitory influences on the respiratory centers may have important implications for premature newborns with apnea as well as older infants at risk for the sudden-infant-death syndrome and possible adults with obstructive sleep apnea.