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The carotid body: A new target for rescuing cardiorespiratory and autonomic imbalance induced by intermittent hypoxia mimicking obstructive sleep apnea

      Background/Aims: We propose that an enhance carotid body (CB) chemosensory drive plays a crucial role in the hypertension and autonomic imbalance induced by chronic intermittent hypoxia (CIH) mimicking obstructive sleep apnea. Thus, we studied the effect of selective CB ablation on the hypertension and autonomic imbalance of rats exposed to CIH. Methods: Male Sprague–Dawley rats (200 g) were submitted to CIH (5% FiO2, 12 times/h, 8 h/day). After 3 weeks, under isofluorane anesthesia both CBs were cryogenically destroyed and rats were kept one more week in CIH. The effectiveness of this maneuver was confirmed by the disappearance of the ventilatory chemoreflex response to iv injection of NaCN. We studied the effects of CB ablation on arterial blood pressure (BP) measured by radio-telemetry (DSI, USA), ventilatory chemoreflex drive (whole body plethysmography), baroreflex sensitivity (BRS), heart rate variability (HRV), arrhythmia index and oxidative stress (TBARS). Results: After 3 weeks of CIH, rats displayed systemic oxidative stress, hypertension, enhanced CB-mediated chemoreflex drive evidence by the potentiation of the hypoxic ventilatory response, a significant reduction in the BRS, predominance of HRV low frequency band, and increased number of cardiac arrhythmic episodes. CB ablation normalized the elevated BP, reduced the enhanced hypoxic ventilatory response, normalized BRS and HRV, and markedly reduced the arrhythmic episodes. On the contrary, systemic oxidative stress was unaffected by CB ablation. Conclusion: We found that cardiorespiratory and autonomic alterations induced by CIH are critically dependent on the enhanced CB chemosensory drive. The CIH-induced hypertension and the autonomic alterations were eliminated by the CB ablation despite of continuous exposure to CIH and higher levels of systemic oxidative stress. Thus, our results show that the CB plays a crucial role in the progression of the CIH-induced hypertension and autonomic imbalance. Supported by FONDECYT 1150040.
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