Cardiorespiratory Alterations Induced by Intermittent Hypoxia in a Rat Model of Sleep Apnea
Cardiorespiratory Alterations Induced by Intermittent Hypoxia in a Rat Model of Sleep Apnea
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DOI：
10.1007/978-1-4419-5692-7_55
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发表时间：
2010-01-01
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影响因子：
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通讯作者：
Del Rio, Rodrigo
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文献类型：
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作者：
Iturriaga, Rodrigo;Moya, Esteban A.;Del Rio, Rodrigo
以间歇性缺氧反复发作为特征的阻塞性睡眠呼吸暂停（OSA）综合征被认为是高血压的独立危险因素。OSA诱发高血压的一个潜在机制是颈动脉体对缺氧的化学感觉反应增强，这是OSA患者和暴露于慢性间歇性缺氧（CIH）的动物对心率变异性（HRV）的交感调节增强和缺氧通气反应增强的原因。然而，目前尚不清楚是否心肺功能改变可能先于高血压。因此，我们研究了OH对暴露于CIH （5% O-2，每8 h 12次/小时）或假手术7-21天的大鼠急性缺氧时动脉压、HRV和通气反应的影响。暴露于CIH 14天后，大鼠对缺氧的通气反应增强，HRV功率谱发生显著变化，以交感调节为主。直到暴露于CIH的第21天，这些心肺功能的改变在动脉血压方面没有明显的变化。因此，我们的研究结果支持这样一种观点，即氯化氢诱导的高血压发生在HRV自主神经平衡改变之前，这与正常血压动物的化学反射性通气反应性增强有关。
The obstructive sleep apnea (OSA) syndrome, characterized by repeated episodes of intermittent hypoxia is recognized as an independent risk factor for hypertension. One potential contributing mechanism to the OSA-induced hypertension is the potentiation of the carotid body chemosensory responses to hypoxia, which is responsible for the augmented sympathetic modulation of heart rate variability (HRV) and the enhanced ventilatory response to hypoxia found in OSA patients and animal exposed to chronic intermittent hypoxia (CIH). However, it is not known if the cardiorespiratory alterations may precede the hypertension. Thus, we studied the effects of OH on arterial pressure, HRV and ventilatory response to acute hypoxia in rats exposed to CIH (5% O-2, 12 times/h per 8 h) or sham condition for 7-21 days. Exposure of rats to CIH for 14 days enhanced the ventilatory response to hypoxia and produced a significant shift of the HRV power spectrum, with a predominance of the sympathetic modulation. These cardiorespiratory alterations occurred without noticeable changes in arterial blood pressure, until 21 days of CIH exposure. Thus, our results support the idea that the hypertension induced by Cl H was preceded by alterations in the autonomic balance of HRV, associated with an enhance chemoreflex ventilatory reactivity in normotensive animals.