Hypoxic ventilatory control in the awake cat five years after carotid body resection.

Steady state breathing patterns, alveolar gases, and arterial blood gases and pH were measured during air, acute hypoxia, and acute hyperoxia in four awake cats 5 years after combined carotid body resection (CBR) and aortic depressor nerve section. Steady state breathing patterns and alveolar gases were also measured in these animals following 3 days of hypoxia (PIO2 = 110 Torr). The results show that the awake cat without carotid bodies and aortic depressor nerves hypoventilates during normoxia in relation to intact cats. Acute hypoxia resulted in respiratory acidosis, decreased tidal volume (VT), and decreased breath duration (TTOT). Exposure to hypoxia for three days resulted in no hyperventilation (isocapnia) but increased VT and TTOT from their levels during acute hypoxia. Acute hyperoxia resulted in respiratory alkalosis and increased VT. Moderate degrees of acute inspiratory hypoxia (FIO2 less than 0.12) induced a behavioral 'arousal' in these cats; this is in direct contrast to the lack of response seen shortly after CBR. Presumably, the recrudescence of chemosensitivity via unsectioned aortic chemoreceptor afferents played a key role in the arousal responses. However, there is no evidence in the cat for recrudescent chemoreceptor input to the respiratory control system with measurable steady state effect. We conclude that the peripheral chemoreceptors are essential for normal resting ventilatory control and for acclimation to chronic hypoxia.