We studied the arousal and ventilatory responses to hypoxia during sleep in three trained dogs, before and 1–4 wk after carotid body denervation (CBD). During the studies the dogs breathed through a cuffed endotracheal tube inserted via a chronic tracheostomy. Eucapnic progressive hypoxia was induced by a rebreathing technique, and arterial O2 saturation (Sao2) was measured with an ear oximeter. Sleep stage was determined by electroencephalographic and behavioral criteria. Following CBD, all dogs exhibited hypoventilation under resting conditions; hypoxic ventilatory responses during wakefulness, slow-wave sleep (SWS), and rapid-eye-movement (REM) sleep were less than 10% of control. Prior to CBD, hypoxic arousal occurred at Sao2 of 83.2 +/- 4.6% (mean +/- Se) during SWS and 70.6 +/-2.2% in REM sleep. Following CBD, arousal failed to occur during progressive desaturation to 60% in SWS and 50% in REM sleep, at which levels hypoxia was arbitrarily terminated. In a few studies following CBD where rebreathing was allowed to continue, the dogs occasionally failed to arouse at all and require active resuscitation. The results indicate a critical role for the carotid chemoreceptors in mediating the arousal response to hypoxia.
Carotid body denervation does not affect CO2 sensitivity in multiple rat strains