Laboratorio de Neurobiología, P. Universidad Católica de Chile, Santiago, Chile.
Adv Exp Med Biol. 2010;669:271-4. doi: 10.1007/978-1-4419-5692-7_55.
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 CIH 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 CIH was preceded by alterations in the autonomic balance of HRV, associated with an enhance chemoreflex ventilatory reactivity in normotensive animals.
阻塞性睡眠呼吸暂停（OSA）综合征的特征是反复间歇性缺氧，被认为是高血压的独立危险因素。OSA 引起的高血压的一个潜在机制是颈动脉体化学感受器对缺氧反应的增强，这导致 OSA 患者和暴露于慢性间歇性低氧（CIH）的动物的心率变异性（HRV）的交感神经调制增强和对缺氧的通气反应增强。然而，尚不清楚心血管改变是否可能先于高血压发生。因此，我们研究了 CIH 对动脉压、HRV 和急性低氧通气反应的影响，在 CIH（5% O（2），12 次/小时，每次 8 小时）或假条件下暴露于 CIH 的大鼠中持续 7-21 天。14 天的 CIH 暴露增强了对缺氧的通气反应，并产生了 HRV 功率谱的显著变化，以交感神经调制为主。这些心肺变化在动脉血压没有明显变化的情况下发生，直到 CIH 暴露 21 天。因此，我们的结果支持了这样的观点，即 CIH 引起的高血压是由 HRV 自主平衡的改变引起的，这与正常血压动物的化学感受器反射性通气反应增强有关。
