Stimulatory and persistent effect of acute hyperoxia on respiratory gas exchange of the chick embryo.
The hypothesis that oxygen availability limits growth of the normal chick embryo late in development predicts that an increase in oxygen availability would accelerate the rate of growth and, therefore, metabolism. We tested the prediction concerning metabolism by comparing the oxygen consumption (VO2) and carbon dioxide production (VCO2) of 14-18 day embryos acutely exposed to either 50% or 100% O2 with those of normoxic (21% O2) controls. Two hours of hyperoxia produced increases in both VO2 and VCO2; however, repeated measurements over time in normoxia also demonstrated a significant increase in gas exchange, presumably due to normal growth of the embryos. After correcting for the increase in VO2 due to growth, there was no effect of 60% O2 on day 14. Thereafter the stimulatory effect of 60% O2 increased gradually, reaching 6.1% on day 18. VCO2 was 4 to 6% higher in embryos acutely exposed to 60% O2 than in normoxic controls throughout the observation period, although the difference was significant only on day 18. The VO2 of embryos acutely exposed to 100% O2 was not significantly different from that observed in 60% O2, and was still significantly elevated 3 h after the eggs were returned to 21% O2. We conclude that acute hyperoxia late in incubation elicits an increase in embryonic VO2 and VCO2, with little or no effect on the respiratory exchange ratio, and that the stimulation of gas exchange by 100% O2 persists after the embryo is returned to normoxic conditions. These findings support the hypothesis that oxygen availability limits growth and metabolism of the normoxic chick embryo late in development.
D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002642:Chick Embryo; D006128:Growth / Q000187:drug effects; D010100:Oxygen / Q000494:pharmacology*; D010101:Oxygen Consumption; D011659:Pulmonary Gas Exchange / Q000187:drug effects*; D013997:Time Factors
D002245:Carbon Dioxide; D010100:Oxygen