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缺氧和高碳酸血症引起的交感神经激活——对睡眠呼吸暂停的影响

Sympathetic activation by hypoxia and hypercapnia--implications for sleep apnea.

作者信息

Somers V K, Mark A L, Abboud F M

机构信息

Department of Internal Medicine, Veterans Administration Medical Center, Iowa City, Iowa.

出版信息

Clin Exp Hypertens A. 1988;10 Suppl 1:413-22. doi: 10.3109/10641968809075998.

DOI:10.3109/10641968809075998
PMID:3072127
Abstract

In normal humans, both hypoxia and hypercapnia result in sympathetic nerve activation, and when combined, i.e. hypoxic hypercapnia, synergistically increase sympathetic activity. Apnea during the hypoxic and hypercapnic stress results in further increases in sympathetic activity. Borderline hypertensive humans have exaggerated sympathetic nerve responses to hypoxia. Hypertensives are also prone to sleep apnea. We suggest that sleep apnea may result in very high levels of sympathetic activity which may contribute to daytime hypertension and/or precipitate cardiovascular catastrophe in hypertensive people during sleep.

摘要

在正常人体中,低氧和高碳酸血症都会导致交感神经激活,而当二者同时存在时,即低氧性高碳酸血症,会协同增加交感神经活动。在低氧和高碳酸血症应激期间出现的呼吸暂停会导致交感神经活动进一步增加。临界高血压患者对低氧的交感神经反应过度。高血压患者也容易出现睡眠呼吸暂停。我们认为,睡眠呼吸暂停可能导致交感神经活动水平极高,这可能会导致白天高血压,和/或在睡眠期间促使高血压患者发生心血管灾难。

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