CAROTID CHEMO--BARORECEPTORS ROLE IN APNEA & HYPERPNEA

我们开发了一种独特的未麻醉动物模型， 颈动脉窦区可以独立于动脉窦区分离和灌注。 体循环与血气、灌注压和化学 由调查人员控制。 这将使我们能够测试 特异性颈动脉化学和压力感受器刺激的缓解作用 单独或与全身（因此CNS）变化联合 化学或血压。 我们将讨论三个具体问题; 1. 颈动脉化学感受器刺激（生理水平的K+， 去甲肾上腺素、乳酸）和/或它们的相互作用有助于 运动性呼吸过度？ 血气有净化作用吗 振荡？ 这些刺激如何与低碳酸血症相互作用？ 2. 中枢神经系统缺氧本身对 呼吸和呼吸肌的大小、稳定性和时间 招募？ 中枢神经系统缺氧是否有助于“滚降”？ CNS是否缺氧 影响化学感受器传入输入的中枢整合？ CNS是否 缺氧影响上呼吸道肌肉的相对募集？ 有没有 睡眠状态的影响？ 中枢神经系统缺氧是否在周期性 呼吸？ 3. 颈动脉血压的短暂生理变化 鼻窦导致不稳定呼吸、中枢性呼吸暂停和/或 上气道阻力 压力感受器和 化学感受器反馈 我们的新动物模型使我们能够研究 在一个完整的准备涉及心肺控制反射 在清醒、睡眠的所有阶段和锻炼期间的反馈增益。 这些反射与上呼吸道的控制有直接关系 通畅性、气体交换和血压，尤其是在睡眠期间，以及 应该提供了深入了解睡眠障碍的病理生理学， 呼吸了 对体力活动的呼吸过度是最常见的 生理性呼吸过度，但其机制尚不清楚 明白 我们的研究，在一个生理模型与完整的反馈， 收益，也应该回答有关的几个基本问题， 控制运动性呼吸过度。

We have developed an unique unanesthetized animal model in which the carotid sinus region can be isolated and perfused independently of the systemic circulation with blood gases, perfusion pressure, and chemistry controlled by the investigators. This will allow us to test the ventilatory effects of specific carotid chemo- and baroreceptor stimuli separately or in conjunction with changes in systemic (and therefore CNS) chemistry or blood pressure. We will address three specific questions; 1. Do carotid chemoreceptor stimuli (physiological levels of K+, norepinephrine, lactic acid) and/or their interactions contribute to exercise hyperpnea? Is there a ventilatory effect of blood gas oscillations? How do these stimuli interact with hypocapnia? 2. What is the effect of central nervous system hypoxia, by itself, on magnitude, stability, and timing of breathing and respiratory muscle recruitment? Does CNS hypoxia contribute to "roll off"? Does CNS hypoxia affect central integration of chemoreceptor afferent input? Does CNS hypoxia affect the relative recruitment of upper airway muscles? Is there an effect of sleep state? Does CNS hypoxia play a role in periodic breathing? 3. Can transient, physiological changes in blood pressure at the carotid sinus contribute to unstable breathing, central apnea, and/or changes in upper airway resistance? Is there interaction between baroreceptor and chemoreceptor feedback? Our new animal model gives us the ability to study fundamental aspects of reflexes involved in cardiorespiratory control in a preparation with intact feedback gains during wakefulness, all stages of sleep, and exercise. These reflexes have direct relevance to the control of upper airway patency, gas exchange, and blood pressure, especially during sleep, and should provide insights into the pathophysiology of sleep disordered breathing. Hyperpnea in response to physical activity is the most common physiological hyperpnea of all, yet its mechanisms are still not well understood. our studies, in a physiological model with intact feedback gains, should also answer several fundamental questions concerning the control of exercise hyperpnea.