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

乙醇抑制对高碳酸血症和缺氧的呼吸反应， 即使是在社交饮酒者中常见的血液酒精水平（巴尔斯）。 睡眠同样会抑制对缺氧的呼吸反应， 高碳酸血症 有害的，对呼吸的相互影响， 不可避免的生理状态的睡眠和广泛使用的物质 在美国，乙醇的使用可能导致严重的发病率和死亡率。 States. 这一修订后的申请扩大了生产性研究计划的乙醇 以及睡眠时呼吸的控制。 我们之前的研究表明 在年轻男性中，乙醇会增加吸气阻力， 同时呼吸驱动的一些测量被抑制。 一大特色 我们计划的一项研究是对绝经后妇女的研究。 的 评估这一人群的基本原理是，女性激素似乎 保护绝经前妇女免受睡眠呼吸障碍。 然而，在这方面， 绝经后妇女没有得到这样的保护，这表明一些最小的 女性荷尔蒙的水平是必要的保护。 因此电流 我们工作的一个阶段侧重于年龄和性别对 睡前酒精后睡眠呼吸。 我们将研究三个 受试者组：1）55 - 75岁的男性; 2） 绝经后妇女（年龄55-75岁）接受激素替代疗法; 3） 绝经后妇女（年龄55-75岁）未接受激素替代治疗。 测量将包括吸气闭塞压，总 呼吸阻力和对高碳酸血症的缓解反应， 等二氧化碳性缺氧 此外，我们还将观察到 呼吸抑制（周期性呼吸、呼吸不足或呼吸暂停， 去饱和）。 我们将检验以下假设： 1.乙醇导致上呼吸道阻力增加， 睡眠在老年男性和老年女性比我们以前研究的年轻 男人 2.乙醇引起中枢化学感受器更明显的减少 老年男性和老年女性的动力表现为反应减弱 比我们之前研究的年轻男性更容易患上高氧高碳酸血症。 3.在男性中，与年龄相关的吸气阻力增加将是 大于乙醇相关的化学感受器驱动抑制， 净效应将是P0.1和高碳酸血症的增加， 反应高于年轻男性。

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.