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David Read Laboratory, Department of Medicine, University of Sydney, 2006 New South Wales, Australia; and Schlafmedizinisches Labor, Department of Medicine, University of Marburg, 35033 Marburg, Germany
Received 17 April 1995; accepted in final form 4 June 1996.
Becker, Heinrich F., Olli Polo, Stephen G. McNamara, Michael
Berthon-Jones, and Colin E. Sullivan. Effect of different levels
of hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683-1690, 1996.
We
have recently shown that breathing 50%
O2 markedly stimulates ventilation
in healthy subjects if end-tidal PCO2
(PETCO2) is
maintained. The aim of this study was to investigate a
possible dose-dependent stimulation of ventilation by
O2 and to examine possible
mechanisms of hyperoxic hyperventilation. In eight normal
subjects ventilation was measured while they were breathing 30 and 75%
O2 for 30 min, with
PETCO2 being held constant.
Acute hypercapnic ventilatory responses were also tested in these
subjects. The 75% O2 experiment
was repeated without controlling
PETCO2 in 14 subjects, and
in 6 subjects arterial blood gases were taken at baseline and at the
end of the hyperoxia period. Minute ventilation
(
I) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75%
O2 without any control on
PETCO2 led to
a 16% increase in
I, but
PETCO2 decreased by
3.6 Torr (9%). There was a linear correlation
(r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, with
I more than doubling after 30 min of
75% O2. If isocapnia is not
maintained, hyperventilation is attenuated by a decrease in arterial
PCO2. There is a correlation between
hyperoxic and hypercapnic ventilatory responses. On the basis of data
from the literature, we concluded that the Haldane effect seems to be
the major cause of hyperventilation during
both isocapnic and poikilocapnic
hyperoxia.
oxygen; ventilatory response; respiration; Haldane effect
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