Role of carotid chemoreflex in respiratory acclimatization to hypoxemia in goat and sheep.

The role of the carotid body chemoreflex in the ventilatory acclimatization to chronic hypoxia was studied in the unanesthetized goat and sheep. The time-cours of changes in ventilation, PCO2, pH and PO2 of arterial blood and cisternal fluid (CF) were measured before and following exposure to a simulated altitude of 3660-5000 m, with and without intact carotid sinus nerves. At sea level, after section of carotid sinus nerves most animals hypoventilated chronically, and developed mild arterial hypoxemia and hypercapnia. Upon exposure to acute hypoxia, all of the intact animals hyperventilated and CF pH increased from 7.310 to 7.380 whereas after chemodenervation, the increase in ventilation was small and delayed, and CF pH decreased from 7.285 to 7.143. During exposure of the intact animals to chronic hypoxia, hyperventilation accompanied by decreases in arterial and CF P CO2 reached its peak in two days; these changes partially subsided during the next few days. Partial compensation of respiratory alkalosis occurred during the first day. In contrast, several chemodenervated animals died during chronic hypoxia; the survivors showed either a small decrease or an increase in Pa CO2. Thus, an intact peripheral chemoreflex drive during hypoxia is necessary for ventilatory acclimatization which raises the arterial and presumably tissue PO2 in spite of alkalosis. The new proposal is that a central tissue metabolic acidosis resulting from a direct effect of acute hypoxia is partly compensated as hypoxia is prolonged. This central compensation decreases ventilatory drive and hence opposes the ventilatory acclimatization during chronic hypoxia initiated by the peripheral chemoreflexes.