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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© 2015 Published by Elsevier Inc.