Journal of Applied Physiology, Vol 46, Issue 5 973-977, Copyright © 1979 by American Physiological Society
Circulatory response to arterial hyperoxia
Y. Cassuto and L. E. Farhi
We have studied the circulatory response to 100% O2 at 1 and 3 atm, using
unanesthetized rabbits in which a systemic artery and the right heart had
been cannulated previously. One group of animals served as controls; the
other was infused with a flurocarbon emulsion that boosted blood O2
solubility to approximately 5 ml.100 ml-1.atm-1. Exposure to hyperoxia
caused an identical sustained rise in arterial PO2 in both groups. O2
uptake was measured during normobaric exposure to 100% O2 and was found to
be the same as in control conditions. There was an immediate rise in right
heart PO2, more marked in infused animals, but this increase was only
temporary, and PO2 dropped, while the right heart-arterial PCO2 difference
rose, indicating a gradual fall in cardiac output. This readjustment
occurred at a faster rate in the infused animals, a difference that led us
to conclude that the peripheral response to hyperoxia is influenced by
factors other than arterial PO2. The pronounced decrease in cardiac output
seen in infused rabbits was accompanied by lactic acidosis, implying that
some of the animals' tissues were becoming hypoxic in the presence of
arterial hyperoxia.
