SLEEP DISORDERED BREATHING AND NEUROCIRCULATORY CONTROL

睡眠呼吸紊乱和神经循环控制

• 批准号: 2609386
• 负责人: BARBARA J MORGAN
• 金额: $ 8.93万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-12-15 至 2000-11-20
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2609386
• 关键词: adenosine; baroreceptors; clinical research; human subject; human therapy evaluation; hypoxia; lung transplantation; neurogenic hypertension; neuroregulation; respiratory therapy; sleep apnea; sympathetic nervous system; vasomotion

Sleep disordered breathing (apnea, hypopnea, and high upper airway resistance) has emerged as an independent risk factor for hypertension. The goal of this project is to determIne the mechanisms by which sleep disordered breathing causes acute and chronic blood pressure elevation in humans. We propose that intermittent asphyxia during sleep raises blood pressure via an increase in sympathetic vasomotor outflow to the peripheral circulation. Aim l will examine the mechanisms by which exposure to asphyxia causes persistent sympathetic activation which outlasts the chemical stimuli. We hypothesize that hypoxia, acting systemically or at the carotid chemoreceptor, triggers this response. Aim 2 will investigate the cause of dissociation between sympathetic vasomotor outflow and vascular resistance during exposure to asphyxia. We propose that adenosine, via direct and indirect vasodilator effects, is responsible for this phenomenon. Aims 3 and 4 will examine mechanisms for neurocirculatory responses to apnea. We hypothesize that the acute pressor response is critically dependent on sympathetic nervous system activation but not on elimination of input from pulmonary stretch receptors. Aim 5 will determine the effects of long- term nasal continuous airway pressure treatment on blood pressure in individuals with mild to moderate sleep disordered breathing. We expect that our experiments will provide explanations for the sympathetic overactivity and hypertension seen in individuals with sleep disordered breathing and, in turn, lead to a more rational approach to therapy.

睡眠障碍呼吸(呼吸暂停、低呼吸和上呼吸道高位 抵抗力)已成为高血压的独立危险因素。 这个项目的目标是确定睡眠的机制 呼吸紊乱导致急性和慢性血压升高 在人类身上。我们认为睡眠中的间歇性窒息会增加 血压通过交感血管运动流出增加到 外周循环。目的L将探讨 暴露在窒息中会引起持续性的交感神经激活， 比化学刺激更持久。我们假设缺氧，表现为 系统地或在颈动脉化学感受器上触发这种反应。 目标2将调查交感神经之间分离的原因 窒息期间的血管运动流出和血管阻力。 我们认为，腺苷通过直接和间接的血管扩张作用， 对这一现象负有责任。目标3和目标4将检查 呼吸暂停的神经循环反应机制。我们假设 急性升压反应严重依赖于交感神经 神经系统激活，但不是基于消除来自 肺伸展感受器。目标5将确定长期- 长期鼻腔持续气道压治疗对高血压患者血压的影响 轻至中度睡眠的个体呼吸障碍。我们预计 我们的实验将为同情的人提供解释 睡眠障碍患者的过度活动和高血压 呼吸，进而导致一种更理性的治疗方法。