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Why is sleep apnea syndrome a risk factor for cardiovascular diseases in adults?

为什么睡眠呼吸暂停综合征是成人心血管疾病的危险因素？

基本信息

批准号：
12670578
负责人：
KUWAHIRA Ichiro
金额：
$ 2.11万
依托单位：
Tokai University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12670578/
关键词：
sleep apnea syndrome intermittent hypercapnic hypoxia lung function hypertension activated platelet animal model sympathetic nervous system parasympathetic nervous system 睡眠無呼吸症候群間歇的低酸素間歇的高炭酸ガス循環呼吸

项目摘要

We investigated the effects of repetitive hypercapnic hypoxia on arterial blood pressure, heart rate, hemoglobin concentration and RV/(LV+S) in rats. Thirty-two male Sprague-Dawley rats were divided into 4 groups, controls, 3 weeks, 4 weeks and 5 weeks exposure group. With the use of a timed solenoid valve, a mixture of CO2 and N2 was flushed into the chamber for 1 min, reducing FIO2 to 7% and raising FICO2 to 8%; then air was flushed allowing return of gas fractions to ambient levels for 3 min. Each cycle was repeated for 6 h/day. Measurements were carried out in the conscious resting state. In all groups, hypercapnic hypoxia decreased Pao2 to 44-46 Torr and increased Paco2 to 48-49 Torr. There was no significant, difference in baseline blood pressure, heart rate, hemoglobin concentration and arterial blood gases among groups. However, arterial blood pressure increased and heart rate decreased significantly during hypercapnic hypoxia, and the magnitude of the changes was highest in the 5 weeks exposure group. Hemoglobin concentration increased transiently during hypercapnic hypoxia in the exposure groups. RV/(LV+S) increased with an increase in the exposure period. Phentolamine attenuated acute blood pressure elevation and atropine abolished bradycardia during hypercapnic hypoxia. The results indicate that this level of repetitive hypercapnic hypoxia does not produce permanent hypertension and polycythemia but induces acute blood pressure elevation, bradycardia and RV hypertrophy which is dependent on the exposure period. Hemoglobin concentration increased transiently during hypercapnic hypoxia. An increased sympathetic and parasympathetic tone seems to play a major role in the development of cardiovascular changes during hypercapnic hypoxia. In addition to hypoxia CO2 retention might play a significant role in the development of cardiovascular changes in patients with sleep apnea syndrome.

本文观察了重复性高碳酸性低氧对大鼠动脉血压、心率、血红蛋白浓度和RV/（LV+S）的影响。雄性SD大鼠32只，随机分为对照组、染毒3周组、染毒4周组和染毒5周组。使用定时电磁阀，将CO2和N2的混合物冲入腔室1分钟，将FIO 2降低至7%，将FICO 2升高至8%;然后冲洗空气，使气体馏分返回环境水平3分钟。每个循环重复6小时/天。测量在有意识的静息状态下进行。在所有组中，高碳酸性缺氧将Pao 2降低至44-46 Torr，并将Pao 2增加至48-49 Torr。各组间基线血压、心率、血红蛋白浓度和动脉血气无显著差异。但在高碳酸性缺氧时，动脉血压升高，心率下降，且变化幅度在5周暴露组中最大。血红蛋白浓度在高碳酸性低氧暴露组一过性升高。RV/（LV+S）随暴露时间的增加而增加。酚妥拉明可减轻高碳酸性缺氧引起的急性血压升高，阿托品可消除高碳酸性缺氧引起的心动过缓。结果表明，这种水平的重复性高碳酸血症缺氧不会产生永久性高血压和红细胞增多症，但会诱导急性血压升高、心动过缓和RV肥大，这取决于暴露时间。血红蛋白浓度在高碳酸血症缺氧时一过性升高。交感神经和副交感神经张力的增加似乎在高碳酸血症缺氧时心血管变化的发展中起主要作用。除缺氧外，CO2潴留可能在睡眠呼吸暂停综合征患者的心血管变化中起重要作用。