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慢性间歇性低氧期间,交感神经压力反射的重置与高血压的发生有关。

Resetting of the sympathetic baroreflex is associated with the onset of hypertension during chronic intermittent hypoxia.

机构信息

Department of Integrative Physiology, Cardiovascular Research Institute, University of North Texas Health Science Centre, 3500 Camp Bowie Blvd, Fort Worth, TX 76107, USA.

出版信息

Auton Neurosci. 2013 Jan;173(1-2):22-7. doi: 10.1016/j.autneu.2012.10.015. Epub 2012 Nov 17.

Abstract

Chronic intermittent hypoxia (CIH) is a model of arterial hypoxemia that accompanies sleep apnea and increases resting arterial pressure (AP). We examined the effects of 7 days of exposure to CIH on arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) in rats. Sprague-Dawley rats (15±2 weeks old) were exposed to CIH (9% oxygen for 3 min every 10 min, 8 h per day) for 7 days (n=16) while control rats (n=18) were maintained in normoxia. Baroreflex regulation of RSNA and HR were estimated in Inactin anesthetized and artificially ventilated rats during infusions of phenylephrine and nitroprusside to manipulate AP. After exposure to CIH, resting mean AP was higher in CIH than that in control group (115±7 vs. 105±7, P<0.001). Resting HR did not differ between the two groups. Exposure to CIH shifted the AP-RSNA relationship rightward (approximately 10 mm Hg, P<0.01). CIH did not alter maximum gain of the baroreflex control of RSNA (-2.6±0.6 vs. -2.5±0.6 arbitrary units (a.u.)/mm Hg) and HR (-1.8±0.6 vs. -1.8±0.7 bpm/mm Hg, CIH vs. control). In addition, cardiac spontaneous baroreflex sensitivity in conscious rats (n=8) also did not change during exposure to CIH. These results indicate that resetting of the sympathetic baroreflex control, rather than an impairment of its sensitivity, is associated with an onset of hypertension induced by CIH.

摘要

慢性间歇性低氧(CIH)是一种伴随睡眠呼吸暂停的动脉低氧血症模型,会增加静息动脉压(AP)。我们研究了 7 天 CIH 暴露对大鼠肾交感神经活动(RSNA)和心率(HR)的动脉压力反射控制的影响。15±2 周龄的 Sprague-Dawley 大鼠(n=16)接受 7 天 CIH(每 10 分钟 9%氧气 3 分钟,每天 8 小时),而对照组大鼠(n=18)保持在常氧环境中。在麻醉并人工通气的大鼠中,通过输注苯肾上腺素和硝普钠来操纵 AP,以评估 RSNA 和 HR 的压力反射调节。暴露于 CIH 后,CIH 组的静息平均 AP 高于对照组(115±7 对 105±7,P<0.001)。两组的静息心率没有差异。CIH 暴露使 AP-RSNA 关系向右移动(约 10mmHg,P<0.01)。CIH 并未改变 RSNA 压力反射控制的最大增益(-2.6±0.6 对 -2.5±0.6 任意单位(a.u.)/mmHg)和 HR(-1.8±0.6 对 -1.8±0.7 bpm/mm Hg,CIH 对对照)。此外,在 CIH 暴露期间,在清醒大鼠(n=8)中,心脏自主压力反射敏感性也没有变化。这些结果表明,与 CIH 引起的高血压相关的是交感神经压力反射控制的重置,而不是其敏感性的损害。

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