ALCOHOL, BREATHING, AND SLEEP--AGE AND GENDER EFFECTS

乙醇抑制了对高碳酸血症和低氧的呼吸反应， 即使是在社交饮酒者常见的血液酒精水平(BAL)下也是如此。 睡眠同样会抑制对缺氧的呼吸反应，并 高碳酸血症。有害的，相互作用的对呼吸的影响 睡眠不可避免的生理状态和广泛使用的物质 在美国，酒精可能是导致显著发病率和死亡率的原因 各州。 这项修订后的申请扩大了关于乙醇的生产性研究计划。 以及睡眠时呼吸的控制。我们之前的工作表明 在年轻男性中，酒精会增加吸气阻力， 而呼吸动力的一些指标却受到了抑制。一大特点 我们建议的研究之一是对绝经后女性的研究。这个 评估这一群体的理由是，女性荷尔蒙似乎 保护绝经前妇女免受睡眠呼吸障碍的困扰。然而， 绝经后的女性没有那么受到保护，这表明一些最低限度的 女性荷尔蒙水平是保护身体所必需的。因此，当前的 我们工作阶段的重点是年龄和性别对 睡前饮酒后睡眠中的呼吸。我们将研究三个方面 受试者分组：1)55岁至75岁的男性；2) 接受激素替代治疗的绝经后妇女(55-75岁)；3) 绝经后妇女(55-75岁)未接受激素替代治疗。 测量将包括吸气闭塞压力，总 呼吸阻力和对高碳酸血症的呼吸反应 等颅压低氧。此外，我们还将观察到相关的现象 有呼吸抑制(周期性呼吸、低呼吸或呼吸暂停和 去饱和度)。 我们将检验以下假设： 1.酒精引起的上呼吸道阻力在 老年男性和老年女性的睡眠比我们之前研究的更年轻 男人。 2.乙醇引起中枢化学感受器更显著的下降 老年男性和老年女性的驱动力，表现为反应减弱 与我们之前研究的年轻男性相比，他们对高氧性高碳酸血症的影响更大。 3.在男性，与年龄相关的吸气阻力增加将是 比酒精相关的化学感受器驱动和抑制更大 净效应将是P0.1的增加和高碳酸血症 年轻男性的反应超过了它的水平。

Ethanol depresses the respiratory response to hypercapnia and to hypoxia, even at blood alcohol levels (BALs) commonly seen in social drinkers. Sleep likewise depresses respiratory responses to hypoxia and hypercapnia. Deleterious, interactive effects on respiration of the unavoidable physiological state of sleep and the widely used substance of ethanol may underlie significant morbidity and mortality in the United States. This revised application expands a productive research program on ethanol and the control of breathing during sleep. Our previous work has shown that in younger men, inspiratory resistance is increased by ethanol, while some measures of respiratory drive are depressed. A major feature of our proposed research is the study of postmenopausal women. The rationale for evaluating this population is that female hormones seem to protect premenopausal women from sleep disordered breathing. However, postmenopausal women are not so protected, suggesting that some minimal level of female hormones is necessary for protection. Thus, the current phase of our work focuses on the influences of age and gender on respiration during sleep after bedtime ethanol. We will study three groups of subjects: 1) men between the ages of 55 and 75 years; 2) postmenopausal women (age 55-75) on hormone replacement therapy; 3) postmenopausal women (age 55-75) not on hormonal replacement. Measurements will include inspiratory occlusion pressure, total respiratory resistance and ventilatory response to hypercapnia and isocapnic hypoxia. In addition, we will observe phenomena associated with respiratory depression (periodic breathing, hypopneas or apneas and desaturations). We will test the following hypotheses: 1. Ethanol causes greater increases in upper airway resistance during sleep in older men and older women than in our previously studied younger men. 2. Ethanol causes more pronounced decreases in central chemoreceptor drive in older men and older women as manifested by a reduced response to hyperoxic hypercapnia than in our previously studied younger men. 3. In men, the age-related increase in inspiratory resistance will be greater than the ethanol-related depression of chemoreceptor drive and the net effect will be an augmentation in P0.1 and the hypercapnic response above its levels in younger men.