Effect of repetitive hypoxic apnoeas on baroreflex function in humans.
Effect of repetitive hypoxic apnoeas on baroreflex function in humans.
复制标题
重复缺氧呼吸暂停对人类压力感受反射功能的影响。
DOI：
10.1113/jphysiol.2006.108977
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发表时间：
2006
期刊：
影响因子：
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通讯作者：
Ray,ChesterA
中科院分区：
文献类型：
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作者：
Monahan,KevinD;Leuenberger,UrsA;Ray,ChesterA
阻塞性睡眠呼吸暂停患者的压力感受反射功能受损。 We tested the hypothesis that short‐term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in baroreflex function.使用改良的牛津技术测定了 14 名受试者（26 ± 1 岁）的压力感受反射功能。压力反射敏感性（BRS）通过 R-R 间期-收缩压（BP；心迷走 BRS）、心率-收缩压（HR BRS）和肌肉交感神经活动（MSNA）-舒张压（交感 BRS）关系进行量化。 RHA 要求受试者在间歇性缺氧期间每分钟重复呼气末呼吸暂停（20 秒），持续 30 分钟，以加剧氧饱和度下降。 RHA 后，静息时血压和 MSNA 升高。在 RHA 后约 7 分钟（第 1 后）、约 30 分钟（后 2）和约 50 分钟（后 3）测量 BRS，以深入了解反应的时间模式。心迷走神经 BRS（前、后 1、后 2 和后 3 分别为 16.8 ± 1.3、16.5 ± 1.6、17.6 ± 2.0 和 17.4 ± 1.5 ms mmHg−1）、HR BRS（−1.1 ± 0.1、−1.1 ± 0.1、−1.3 ± 0.1 和 −1.4 ± 0.1 RHA 未改变心跳 min−1mmHg−1) 和交感神经 BRS（−4.5 ± 0.6、−4.4 ± 0.7、−3.7 ± 0.5 和 −4.7 ± 1.0 任意单位 (au)beat−1mmHg−1）。相反，RHA 后压力感受反射的工作点向右移动（至较高的血压水平）和向上移动（至较高的心率和 MSNA 水平）（P < 0.05）。对另外五名受试者进行的时间控制研究显示，任何测量变量都没有随时间变化。总的来说，这些数据表明，短期暴露于 RHA 会将压力感受反射刺激-反应曲线移动（“重置”）至更高的血压水平，而不会长时间影响 BRS。
Baroreflex function is impaired in patients with obstructive sleep apnoea. We tested the hypothesis that short‐term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in baroreflex function. Baroreflex function was determined using the modified Oxford technique in 14 subjects (26 ± 1 years). Baroreflex sensitivity (BRS) was quantified from the R‐R interval–systolic blood pressure (BP; cardiovagal BRS), heart rate–systolic BP (HR BRS) and muscle sympathetic nerve activity (MSNA)–diastolic BP (sympathetic BRS) relations. RHA involved subjects performing repetitive end‐expiratory apnoeas (20 s) every minute for 30 min during intermittent hypoxia to accentuate oxygen desaturation. After RHA, BP and MSNA at rest were elevated. BRS was measured ∼7 (Post 1), ∼30 (Post 2) and ∼50 min (Post 3) after RHA to provide insight into the temporal pattern of responses. Cardiovagal BRS (16.8 ± 1.3, 16.5 ± 1.6, 17.6 ± 2.0 and 17.4 ± 1.5 ms mmHg−1for Pre, Post 1, Post 2 and Post 3, respectively), HR BRS (−1.1 ± 0.1, −1.1 ± 0.1, −1.3 ± 0.1 and −1.4 ± 0.1 beats min−1mmHg−1) and sympathetic BRS (−4.5 ± 0.6, −4.4 ± 0.7, −3.7 ± 0.5 and −4.7 ± 1.0 arbitrary units (au) beat−1mmHg−1) were unchanged by RHA. In contrast, the operating points of the baroreflexes were shifted rightward (to higher levels of BP) and upward (to higher levels of heart rate and MSNA) after RHA (P< 0.05). Time control studies performed in five additional subjects showed no change in any of the measured variables over time. Collectively, these data indicate that short‐term exposure to RHA shifts (‘resets’) the baroreflex stimulus–response curve to higher levels of BP without influencing BRS for extended periods of time.