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临界高血压患者交感神经对低氧反应的增强作用。

Potentiation of sympathetic nerve responses to hypoxia in borderline hypertensive subjects.

作者信息

Somers V K, Mark A L, Abboud F M

机构信息

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

出版信息

Hypertension. 1988 Jun;11(6 Pt 2):608-12. doi: 10.1161/01.hyp.11.6.608.

DOI:10.1161/01.hyp.11.6.608
PMID:3391673
Abstract

We tested the hypothesis that sympathetic nerve responses to stimulation of chemoreceptors by hypoxia are exaggerated in borderline hypertensive humans. We compared responses to isocapnic hypoxia in eight borderline hypertensive subjects and eight normotensive control subjects matched for age, sex, weight, and height without a family history of hypertension. Measurements of heart rate, mean blood pressure, minute ventilation, and sympathetic nerve activity to muscle were made before and during hypoxia. We also measured responses to a period of voluntary apnea during hypoxia. There were no significant differences between the increases in heart rate, blood pressure, and ventilation in response to hypoxia in the two groups. However, during hypoxia sympathetic activity in the hypertensive subjects increased by 40.6 +/- 13.6% (mean +/- SE), greater than the increase of 20.4 +/- 5.0% in the control subjects (p less than 0.05). In six hypertensive and six control subjects, when apnea was performed during hypoxia, sympathetic activity increased by 605.0 +/- 294.3% in the hypertensive subjects and by only 52.8 +/- 17.3% in the control subjects (p less than 0.001). We conclude that the chemoreceptor reflex is enhanced in borderline hypertensive subjects and results in exaggerated increases in sympathetic nerve activity during hypoxia. This enhanced chemoreceptor reflex is especially obvious when the inhibitory influence of breathing and thoracic afferent activity is eliminated by apnea. This exaggerated response may contribute to excess sympathetic activity in borderline hypertensive subjects and to adverse consequences of sleep apnea in hypertensive subjects.

摘要

我们验证了这样一个假设

在临界高血压患者中,低氧刺激化学感受器所引发的交感神经反应会被夸大。我们比较了8名临界高血压受试者和8名年龄、性别、体重和身高匹配且无高血压家族史的正常血压对照受试者对等容低氧的反应。在低氧之前和期间,测量了心率、平均血压、分钟通气量以及肌肉交感神经活动。我们还测量了低氧期间一段自主呼吸暂停的反应。两组对低氧反应时心率、血压和通气量的增加没有显著差异。然而,在低氧期间,高血压受试者的交感神经活动增加了40.6±13.6%(平均值±标准误),大于对照受试者增加的20.4±5.0%(p<0.05)。在6名高血压受试者和6名对照受试者中,当在低氧期间进行呼吸暂停时,高血压受试者的交感神经活动增加了605.0±294.3%,而对照受试者仅增加了52.8±17.3%(p<0.001)。我们得出结论,临界高血压受试者的化学感受器反射增强,导致低氧期间交感神经活动过度增加。当呼吸和胸段传入活动的抑制性影响通过呼吸暂停消除时,这种增强的化学感受器反射尤为明显。这种过度反应可能导致临界高血压受试者交感神经活动过度,并导致高血压受试者睡眠呼吸暂停的不良后果。

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