SCOR IN CARDIOPULMONARY DISORDERS OF SLEEP

这项《SCOR更新建议》中提出的研究是针对基本的 睡眠障碍的机制、流行病学和临床后果 呼吸(SDB)及其治疗。 1.我们将调查呼吸事件发生的机制 伴发SDB会导致持续性高血压。假设 颈动脉化学反射敏感性增强会导致慢性抬高 交感血管运动流出和外周血管阻力 将在人体上进行测试，并长期使用仪器睡眠和 麻醉的狗。我们将强调“敏化”的作用 颈动脉化学感受器对持续性、间歇性窒息的反应 持续高血压的主要决定因素。 2.我们将使用熟睡的狗和人来确定那些 启动和维持睡眠诱导的不稳定的机制 呼吸运动输出和中枢性呼吸暂停。我们还将确定 呼吸运动输出抑制和中枢性呼吸暂停对呼吸功能的影响 人类受试者上呼吸道通畅的情况 对上呼吸道阻塞的易感性。 3.我们建议继续研究该病的流行病学，以期 在5-9年的时间跨度内从夜间多导描记中积累数据 在我们800名就业的男性和女性中，他们的性别差异很大。 这些纵向数据将使我们能够解决病理生理学 轻度、无症状系统性红斑狼疮的意义及病因探讨 机械装置。基于我们四年的横断面数据，我们建议 使用纵向研究来关注最重要的特定问题 与公共健康相关，即：老龄化和更年期在 睡眠呼吸暂停综合征的发展及对睡眠障碍的影响 系统性高血压。 4.我们将确定夜间活动的细胞机制 哮喘。我们的具体假设集中在独立的和 睡眠与皮质醇和皮质醇昼夜节律变化的交互作用 肾上腺素对呼吸道、支气管收缩和呼吸道炎症的影响。 5.我们会发展电脑辅助方法，以应用于 高效、准确的SDB分析。具体来说，我们将完成和 扩展我们的睡眠分析程序的开发，以达到以下目的 年发生的心肺事件的计算机量化 并用于分析睡眠状态的不稳定性和连续性。

The research proposed in this SCOR Renewal Proposal is aimed at the basic mechanisms, epidemiology and clinical consequences of sleep disordered breathing (SDB) and its treatment. 1. We will investigate the mechanisms by which the respiratory events which accompany SDB cause sustained hypertension. The hypothesis that an augmented carotid chemo-reflex sensitivity produces chronic elevations in sympathetic vaso motor outflow, and peripheral vascular resistance will be tested in humans and chronically-instrumented sleeping and anesthetized dogs. We will emphasize the role of "sensitization" of the carotid chemoreceptor in response to sustained, intermittent asphyxia as a major determinant of sustained hypertension. 2. We will determine - using the sleeping dog and human - those mechanisms which initiate and perpetuate sleep-induced instability of respiratory motor output and central apnea. We will also determine the influence of inhibition of respiratory motor output and central apnea on patency of the upper airway in human subjects who very widely in their susceptibility to upper airway obstruction. 3. We propose to continue to study the epidemiology of SDB with the aim of accumulating data from over night polysymography over a 5-9 year span in our cohort of 800 employed men and women with a wide range of SDB. These longitudinal data will permit us to address the pathophysiologic significance of mild, asymptomatic SDB and to investigate etiologic mechanisms. Based on our 4 years of cross-sectional data, we propose to use longitudinal studies to focus on specific questions of greatest relevance to public health, namely: the roles of aging and menopause in the development of SDB and the effect of SDB on hypersomnolence and systemic hypertension. 4. We will determine the cellular mechanisms responsible for nocturnal asthma. Our specific hypothesis focuses on the independent and interactive effects of sleep and circadian changes in cortisol and epinephrine on airway broncho-constriction and airway inflammation. 5. We will to develop computer-assisted methods for use in the efficient, accurate analysis of SDB. Specifically we will complete and extend our development of a Sleep Analysis Program for purposes of computer based quantitation of cardio-pulmonary events which occur in sleep and for the analysis of sleep state instability and continuity.