Cardiorespiratory Alterations Induced by Intermittent Hypoxia in a Rat Model of Sleep Apnea

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.