VENTILATORY CONTROL IN PERIPHERAL CHEMORECEPTOR-DENERVATED PONIES DURING CHRONIC HYPOXEMIA

Measurements were made: on 10 ponies near sea level (SL 740 Torr) under normal conditions; on 6 of these at SL following chemoreceptor denervation (CD); and subsequently on all 10 during 4 days of hypobaric hypoxia (PaO2 [arterial O2 tension] = 40-47 Torr). CD resulted in hypoventilation at SL (.DELTA.PaCO2 = +7.8 Torr, P < 0.05), and it prevented hyperventilation normally observed with injection of NaCN and acute exposure to hypoxia (< 1 h). In contrast, hyperventilation was evident in normal ponies during acute hypoxia (.DELTA.PaCO2 = -6.7 Torr). Ventilation increased in both groups between the 2nd and 8th h of hypoxia (.DELTA.PaCO2 from 1 h = -4 Torr, P < 0.05). This change, a common characteristic of acclimatization, persisted throughout 4 days of hypoxia in the normal ponies. In the CD ponies this change was evident consistently only through the 12th h and after the 44 h hyperventilation was no longer evident. The peripheral chemoreceptors are apparently essential in ponies for normal .ovrhdot.VE acclimatization to this degree of hypoxemia. Two additional findings in CD ponies suggest the presence of a CNS inhibitory influence on the .ovrhdot.VE [ventilation] control center during chronic hypoxemia. First, acute hyperoxygenation on the 4th day of hypoxemia induced hyperventilation (.DELTA.PaCO2 = -5 Torr, P < 0.05). Second, again on the 4th day and during hyperoxygenation, .ovrhdot.VE responsiveness to CO2 and doxapram HCl was greater than at sea level.