急性低氧及高二氧化碳刺激对阻塞性睡眠呼吸暂停低通气综合征患者外周动脉硬度及血压的影响  

Effect of acute hypoxia and hypercapnia on arterial stiffness and blood pressure in patients with obstructive sleep apnea hypopnea syndrome

作　　者：吕云辉[1] 何忠明[3] 董霄松[2] 李静[2] 韩旭[2] 安培[2] 王丽[2] 何权瀛[2] 韩芳[2] 

机构地区：[1]云南省第一人民医院呼吸内科,昆明650032 [2]北京大学人民医院呼吸科 [3]新疆克拉玛依市中心医院呼吸内科

出　　处：《中华结核和呼吸杂志》2009年第1期42-45,共4页Chinese Journal of Tuberculosis and Respiratory Diseases

基　　金：国家自然科学基金资助项目（30770938,30300120）

摘　　要：目的探讨急性低氧及高CO2刺激对OSAHS患者外周动脉硬度和血压的影响。方法选取2006年1月至12月到北京大学人民医院睡眠中心进行多导睡眠呼吸牛理监测者，试验组包含呼吸暂停低通气指数（AHI）≥10次／h的OSAHS患者28例，男22例，女6例，平均年龄（40±14）岁；对照组包含26名AHI〈5次／h的健康志愿者，男20名，女6名，平均年龄（40±15）岁，均排除高血压、糖尿病、冠状动脉粥样硬化性心脏病及其他心、肺、血管疾病。两组均按相同方法测定四肢血压及心脏-踝血管指数（CAVI），以清醒平卧休息时为基础值，通过重复呼吸法利川特制的密闭呼吸回路分别进行急性高CO2、低氧、低氧合并高CO2吸入刺激，每次刺激结束后立即重复测定四肢血压及CAVI值。计数资料的对比采用X^2检验，多组间比较采用单因素方差分析，组间两两比较采用t检验。结果两组间基础状态下收缩压、舒张压、平均压及CAVI值比较差异均无统计学意义（t值分别为1．720、1．891、1．828及0．103，均P〉0．05）。给予高CO2刺激后两组CAVI均呈下降趋势，但试验组[（7．3±1．2）m／s]下降的程度与基础状态[（7．3±1．3）m／s]比较差异无统计学意义（t＝0．333，P〉0．05），对照组[（7．0±1．4）m／s]出现明显下降（t=2．587，P〈0．05）；两组的收缩压均明显升高。给予低氧刺激后两组CAVI均呈升高趋势，试验组[（7．3±1．1）m／s]改变不明湿，对照组[（7．6±1．6）m/s]明显升高，差异有统计学意义（t=-3．882，P〈0．01），血压没有明显改变（t值分别为-0．434及-0．400，均P〉0．05）。给予低氧合并高CO2刺激后两组CAVI均呈升高趋势，对照组[（7．5±1．7）m／s]明显升高，但程度较单纯低氧刺激时低，血堆的改变与单纯高CO2刺激时类似。结论CO2升高及低氧均可影响外周动脉硬度。OSAHS患者对低氧�Objective To investigate the effect of acute hypoxia and/or hypercapnia on cardio-ankle vascular index （CAVI） and blood pressure （BP） in patients with obstructive sleep apnea hypopnea syndrome （OSAHS）. Method CAVI and blood pressure were measured before and after isocapnia hypoxic, hyperoxia hypercapnic, and hypoxic and hypercapnic challenge in 28 non-hypertensive patients with OSAHS （AHI〉 10/h） and 26 healthy controls （AHI 〈 5/h）, respectively. They were matched for age and sex. Hypoxia and hypercapnia were induced by re-breathing technique. Results The 2 groups had no differences in regard to systolic （SBP） and diastolic BP（DBP） and CAVI. After hypercapnic challenge, SBP increased significantly in both groups. CAVI decreased significantly in controls, but not in OSAHS. Hypoxia induced significant increase of CAVI, but not in OSAHS. SBP and DBP maintained to the pre-challenge levels in both group. Hypercapnia and hypoxia together caused increase of SBP in both groups, and CAVI increased significantly in controls, but not in OSAHS. Conclusions Acute hypoxia and hypercapnia exposure caused change of arterial stiffness and BP in both control and patients with sleep apnea hypopnea syndrome. However, CAVI responses to hypoxic and/or hypercapnic challenge were blunted in patients with OSAHS.

关 键 词：睡眠呼吸暂停综合征 阻塞性 持续气道止压 

分 类 号：R686[医药卫生—骨科学]