ETHANOL AND RESPIRATORY DRIVE DURING SLEEP

乙醇(E)是一种呼吸抑制剂，呼吸衰竭是 E过量死亡的主要原因。呼吸系统对 E以剂量依赖的方式抑制高碳酸血症和低氧， 即使是在社交饮酒者中常见的血清酒精水平。沉睡 同样会抑制对低氧和高二氧化碳的呼吸反应。它是 未知睡眠和酒精对呼吸的联合作用是什么 驾驶。同样未知的是对这些疾病易感性的可能变化 E对有潜在心肺问题的受试者的影响， 尤其是那些有睡眠相关呼吸道症状的人，如 打呼噜和睡眠呼吸暂停。这一小笔赠款申请是临时基金。 进一步发展一个广泛的关于电子和互联网的合作研究计划 睡眠时呼吸的控制。申请的科学家是新来的 酒精研究领域，但他们在酒精研究方面经验丰富 控制人类在清醒和睡眠期间的呼吸。他们的第一次 关于这一主题的研究表明，在习惯打呼噜的男性中，E 增加上呼吸道阻力(通过鼻腔持续时间测量 消除鼾声所需的气道正压)，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。测量结果将 包括吸气闭塞压、总呼吸阻力和 对高碳酸血症和等二氧化碳低氧的呼吸机能反应 观察与呼吸抑制有关的现象(周期性 呼吸、低呼吸或呼吸暂停及饱和度降低)。这些研究将允许 上呼吸道阻力增加的贡献的区分 而呼吸动力减弱导致睡眠呼吸紊乱的增加 在8名年轻的非肥胖者身上获得了初步结果。 不打呼噜的男人。计划对打鼾者进行进一步研究，年龄较大的正常人 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.