ETHANOL AND RESPIRATORY DRIVE DURING SLEEP

乙醇（E）是一种呼吸系统疾病，呼吸衰竭是一种呼吸系统疾病。 E过量的主要死因呼吸系统对 E以剂量依赖性方式抑制高碳酸血症和缺氧， 即使是在社交饮酒者中常见的血清酒精水平下。睡眠 同样抑制对缺氧和高碳酸血症的呼吸反应。是 不知道睡眠和酒精对呼吸系统的综合影响 驱动同样未知的是对这些的易感性的可能变化 E在有潜在心肺问题的受试者中的作用， 特别是那些具有睡眠相关呼吸症状的受试者， 打鼾和睡眠呼吸暂停。这份小额赠款申请是临时资金 进一步发展一个广泛的合作研究计划，E和 控制睡眠时的呼吸。申请科学家是新的， 酒精研究领域，但他们在酒精研究方面经验丰富， 控制人在清醒和睡眠时的呼吸。他们的第一 这项研究表明，在习惯性打鼾的男性中，E 增加上呼吸道阻力（通过鼻连续测量） 消除打鼾所需的气道正压通气），并可导致睡眠 呼吸暂停他们将通过更灵敏的测量来扩展他们的工作， 适用于不打鼾者的呼吸驱动。测量将 包括吸气阻塞压力、总呼吸阻力 除了对高碳酸血症和等碳酸血症性缺氧的缓解反应外， 观察与呼吸抑制相关的现象（周期性 呼吸、呼吸不足或呼吸暂停和去饱和）。这些研究将使 上气道阻力增加的贡献的区分 和减少呼吸驱动增加睡眠呼吸障碍 由E.初步结果已获得8名年轻的非肥胖 不打鼾的男人计划对打鼾者进行进一步研究， 受试者和轻度阻塞性睡眠呼吸暂停患者。

Ethanol (E) is a respiratory depressant and respiratory failure is the major cause of death in E overdose. The respiratory responses to hypercapnia and to hypoxia are depressed by E in a dose-dependent manner, even at serum alcohol levels commonly seen in social drinkers. Sleep likewise depresses respiratory responses to hypoxia and hypercapnia. It is unknown what are the combined effects of sleep and ethanol on respiratory drive. Also unknown are the possible changes in susceptibility to these effects of E in subjects with underlying cardiopulmonary problems, especially those subjects with sleep-related respiratory symptoms such as snoring and sleep apnea. This small grant application is for interim funds to further develop a broad collaborative research program on E and the control of breathing during sleep. The applicant scientists are new to the field of alcohol research but they are experienced in studies on the control of respiration in humans during wakefulness and sleep. Their first work on this topic demonstrated that in males who habitually snore, E increases upper airway resistance (measured by the nasal continuous positive airway pressure required to eliminate snoring) and can cause sleep apnea. They will extend their work with more sensitive measurements of respiratory drive that are applicable to nonsnorers. Measurements will include inspiratory occlusion pressure, total respiratory resistance and ventilatory response to hypercapnia and isocapnic hypoxia in addition to observation of phenomena associated with respiratory depression (periodic breathing, hypopneas or apneas and desaturations). These studies will allow differentiation of the contributions of increased upper airways resistance and reduced respiratory drive to the increase in sleep disordered breathing produced by E. Preliminary results have been obtained in 8 young nonobese non snoring men. Further studies are planned on snorers, older normal subjects and in patients with mild obstructive sleep apnea.