RESPIRATORY RELATED MOTOR OUTPUT TO UPPER AIRWAY MUSLCES

这项研究是基于一个普遍的假设， 而表现出阶段性呼气活动的咽肌具有 在生理和生理呼吸调节中的重要作用， 病理生理状态。 以前的动物和人类研究， 其他实验室表明喉内收肌积极地帮助 制动呼气调节肺容量和呼气时间。 在 与喉内收肌相比， 控制咽肌时相呼气活动的因素 例如咽缩肌（PC）肌肉及其在 呼吸 有人认为，PC肌肉收缩气道 并且据推测，它们促进上呼吸道闭合， 睡吧 相反，我们假设在咽部条件下， 气道变窄，PC肌肉实际上扩张和扩张气道。 它们的扩张和硬化作用会降低气道闭合压 帮助保持气道通畅。 我们实验室以前的研究已经确定了呼吸- 在人类受试者中的喉内收肌的相关活动。 拟议 在去大脑猫中的方案被设计为测试以下内容 关于喉内收肌控制机制的假说 激活：1）不同的喉内收肌对 肺容量减少，2）相位和紧张性容量反馈调节肺 通过反射性调节运动输出到喉部的呼气期间的体积 内收肌，和3）喉内收肌活动的增加相关 呼气末肺容量减少主要是由以下因素介导的 无髓胸迷走神经传入。 我们的动物模型也将被用来测试以下假设 关于PC肌肉：1）PC表现出与运动相关的活动 并对各种呼吸刺激作出反应; 2）PC激活 使狭窄的咽部气道扩张和变硬。 前 这一假设也将在清醒状态下的正常人类受试者中进行检验 睡觉 为了验证我们的假设，即PC肌肉的激活 在维护上层社会方面， 睡眠期间的气道通畅性，夜间将记录PC活动 阻塞性睡眠呼吸暂停患者的多导睡眠图 气道阻力综合征 拟议方案的初步结果表明， 刺激对喉内收肌的激活有不同的影响， PC肌肉支持我们的假设，即两组上气道 呼气肌在呼吸控制中具有不同的作用。 然而，对于给定的上气道肌肉， 对猫和人类受试者进行去大脑处理。 这种反应的密切相关性 将允许在动物实验中探索可能的机制， 在人类身上进行的潜在观察。

The proposed research is based on the general hypothesis that laryngeal and pharyngeal muscles that exhibit phasic expiratory activity have an important role in the regulation of respiration in physiologic and pathophysiologic states. Previous animal and human studies from this and other laboratories indicate that laryngeal adductor muscles help actively brake exhalation regulating lung volume and the time of expiration. In contrast to the laryngeal adductors, relatively little is known about the factors controlling pharyngeal muscles with phasic expiratory activity such as the pharyngeal constrictor (PC) muscles and their role in respiration. It has been assumed that the PC muscles constrict the airway and it has been speculated that they promote upper airway closure during sleep. In contrast, we hypothesize that under conditions of pharyngeal airway narrowing, PC muscles actually dilate and stiffen the airway. Their dilating and stiffening action would lower airway closing pressure helping to maintain airway patency. Previous studies from our laboratory have determined the respiratory- related activity of laryngeal adductors in human subjects. The proposed protocols in decerebrate cats are designed to test the following hypotheses regarding the mechanisms controlling laryngeal adductor muscle activation: 1) different laryngeal adductors have similar responses to decreased lung volume, 2) phasic and tonic volume feedback regulate lung volume during expiration by reflexly modulating motor output to laryngeal adductors, and 3) the increase in laryngeal adductor activity associated with a decrease in end-expiratory lung volume is primarily mediated by unmyelinated thoracic vagal afferents. Our animal model will also be used to test the following hypotheses regarding the PC muscles: 1) the PCs exhibit respiratory-related activity and respond to a variety of respiratory stimuli, and 2) PC activation dilates and stiffens the narrowed pharyngeal airway. The former hypothesis will also be tested in normal human subjects during wakefulness and sleep. To test our hypothesis that activation of the PC muscles has a protective rather than a punitive role in the maintenance of upper airway patency during sleep, PC activity will be recorded during nighttime polysomnograms in patients with obstructive sleep apnea and high upper airway resistance syndrome. Preliminary results of the proposed protocols indicate that respiratory stimuli have different effects on the activation of laryngeal adductor and PC muscles supporting our hypothesis that the two sets of upper airway expiratory muscles have different roles in the control of respiration. Nevertheless, results for a given upper airway muscle are very similar in decerebrate cats and human subjects. This close correlation in responses will allow an exploration in animal experiments of the possible mechanisms underlying observations made in humans.