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NEURAL SITES MEDIATING OBSTRUCTIVE SLEEP APNEA

NEURAL SITES MEDIATING OBSTRUCTIVE SLEEP APNEA
调节阻塞性睡眠呼吸暂停的神经部位
批准号:
6110978
负责人:
RONALD Marven HARPER
金额:
$23.08万
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-09-01 至 1999-08-31

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中文摘要
翻译
目标是利用功能磁共振来确定 (FMRI)技术,脑激活的位置和时间进程 阻塞性睡眠呼吸暂停时激活的结构。我们假设 眼眶额叶皮质的特定区域,下丘脑吻部, 杏仁核、蓝斑、中缝中线、背侧和腹侧脑桥, 在清醒的对照组受试者中激活为模拟的阻塞性呼吸暂停, 将无法激活,或在睡眠呼吸暂停期间活动减少 患者的事件,但在模拟期间将继续激活 对照组睡眠时发生阻塞性呼吸暂停。参与的其他地区 抑制肌肉张力可能表明患者过度激活, 从而导致阻塞性呼吸暂停。由30次重复组成的时间序列 横跨整个大脑的图像切片将在矢状面获得 使用血氧水平依赖(BOLD)回声平面成像脉冲的平面 20例梗阻性病变的最佳血流灌注检测序列 呼吸暂停患者和20名年龄和性别匹配的对照组 睡眠(患者)和在吸气负荷(20厘米水)期间施加 睡眠时开始吸气(对照组)。进行分区 睡眠的影响,两组都将进行基线清醒记录, 然后是吸气负荷和瓦尔萨尔瓦加压挑战者,这 模拟阻塞性呼吸暂停的感觉和自主神经方面。心率, 血流、无创血压、手臂出汗和数字血氧仪将 与图像扫描同时测量。MR信号的变化将是 使用针对功能磁共振成像处理进行优化的软件进行评估,以衡量区域 呼吸暂停事件、吸气负荷和呼吸暂停期间的激活变化 富有同情心的挑战。区域形象变化的交叉相关性与 呼吸、心血管和交感神经流出的诱因 计算出来的。这些研究有可能识别大脑区域。 参与调节上呼吸道张力障碍,以提供对 阻塞性睡眠呼吸暂停的药物干预 参与呼吸道阻塞自主神经伴发的神经部位。
英文摘要
The objectives are to determine, using functional magnetic resonance (fMRI) techniques, the location and time course of activation of brain structures activated during obstructive sleep apnea. We hypothesize that particular regions of the orbital frontal cortex, rostral hypothalamus, amygdala, locus coeruleus, midline raphe, and dorsal and ventral pons, which activate to simulated obstructive apnea in waking control subjects, will fail to activate, or respond with reduced activity during sleep apnea events of patients, but will continue to activate during simulated obstructive apnea during sleep in controls. Other regions involved in the suppression of muscle tone may show excessive activation in patients, thereby inducing obstructive apnea. A time series of 30 repetitions of 20 image slices across the entire brain will be obtained in the sagittal plane using blood oxygen level dependent (BOLD) Echo Planar-Imaging pulse sequences, optimal for sensing perfusion alterations, in 20 obstructive apnea patients and 20 age- and sex-matched controls during apnea events of sleep (patients) and during inspiratory loads (20 cM water) applied at the onset of an inspiratory effort during sleep (controls). To partition effects of sleep, both groups will undergo a baseline waking recording, followed by inspiratory loading, and Valsalva pressor challengers, which simulate sensory and autonomic aspects of obstructive apnea. Heart rate, flow, non-invasive blood pressure, arm sweating, and digit oximetry will be measured concurrently with image scans. The MR signal changes will be assessed with software optimized for fMRI processing to gauge regional activation changes during apneic events, inspiratory loading and sympathetic challenges. Cross correlations of regional image changes with respiratory, cardiovascular and sympathetic outflow induces will be calculated. The studies have the potential to identify brain regions involved in mediating upper airway atonia, to provide insights into pharmacologic intervention for obstructive sleep apnea, and to determine the neural sites involved in autonomic concomitants of airway obstruction.
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