Effect of 100% O2 on hypoxic eucapnic ventilation.
We measured ventilation in nine young adults while they breathed pure O2 after breathing room air and after 5 and 25 min of hypoxia. With isocapnic hypoxia (arterial O2 saturation 80 +/- 2%) mean ventilation increased at 5 min and then declined, so that at 25 min values did not differ from those on room air. After 3 min of O2 breathing, ventilation was greater than that on room air or after 25 min of isocapnic hypoxia, whether the hyperoxia had been preceded by hypoxia or normoxia. During transitions to pure O2 breathing, ventilation was analyzed breath by breath with a moving average technique, searching for nadirs before and after increases in PO2. After both 5 and 25 min of hypoxia, O2 breathing was associated with transient depressions of ventilation, which were greater after 25 min than after 5 min. Significant depressions were not observed when hyperoxia followed room air breathing, and O2-induced nadirs after hypoxia were lower than those observed during room air breathing. O2 transiently depressed ventilation after hypoxia but not after room air breathing. These results suggest that the normal ventilatory response to isocapnic hypoxia has two components, an excitatory one from peripheral chemoreceptors, which is turned off by O2 breathing, and a slower inhibitory one, probably of central origin, which is affected less promptly by O2 breathing.
Holtby
S G
SG
Department of Medicine, University of Manitoba, Winnipeg, Canada.
Berezanski
D J
DJ
Anthonisen
N R
NR
D000328:Adult; D002248:Carbon Monoxide / Q000097:blood; D002344:Carotid Body / Q000502:physiology; D002628:Chemoreceptor Cells / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D010100:Oxygen; D012119:Respiration; D013997:Time Factors
D002248:Carbon Monoxide; D010100:Oxygen