Carotid bodies are required for ventilatory acclimatization to chronic hypoxia

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Abstract
We have compared the ventilatory responses of intact and carotid body-denervated (CBD) goats to moderate [partial pressure of O2 in arterial blood; (PaO2) .apprx. 44 Torr] and severe (PaO2 .apprx. 33 Torr) hypoxemia at many time points for up to 7 days of hypobaria. In the intact group there were significant time-dependent decreases in partial pressure of CO2 in arterial blood (PaCO2) in both moderate and severe hypoxemia (.apprx. -7 and -11 Torr) that were largely complete by 8 h of hypoxemia and maintained throughout. Acute restoration of normoxia in chronically hypoxic intact animals produced time-dependent increases in PaCO2 over 2 h, but hypocapnia persisted relative to sea-level control. Arterial plasma [HCO3-] and [H+] decreased, and [Cl-] increased with a time course and magnitude consistent with developing hypocapnia. Chronic CBD, per se, resulted in a sustained, partially compensated respiratory acidosis, as PaCO2 rose 6 Torr and base excess rose 3 mEq/l, [Cl-] fell 1 mEq/l, and pHa fell 0.01 units. During exposure to identical levels of arterial hypoxemia as in the intact group, CBD animals showed no significant changes in PaCO2, [H+]a, or [HCO3-]a at any time during moderate or severe hypoxemia. Plasma [Cl-] remained within the normal range throughout exposure to moderate hypoxia and increased in severe hypoxia. In a few instances some hypocapnia was observed, but this was highly inconsistent and was always less than one-third of that observed in intact goats. In contrast to intact goats, acute restorations of normoxia in the chronically hypoxic CBD goats always caused hyperventilation. We conclude that carotid bodies are required for ventilatory acclimatization and for any significant hyperventilatory response to hypoxemia over a very wide range of severity and duration of hypoxic exposure. These results suggest that brain [H+] does not play a crucial role in this ventilatory response.