Effect of different levels of hyperoxia on breathing in healthy
subjects.
Becker, Heinrich F., Olli Polo, Stephen G. McNamara, Michael Berthon
-Jones, and Colin E. Sullivan.
Department of Medicine, David Read Laboratory, University of
Sydney, 2006 NSW, Australia, University of Marburg, Dep. of Medicine,
Schlafmedizinisches Labor, 35033 Marburg, Germany
APStracts 3:0279A, 1996.
We have recently shown that breathing 50% oxygen 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 oxygen and to
examine possible mechanisms of hyperoxic hyperventilation. In 8
normal subjects ventilation was measured while breathing 30% and 75%
O2 for 30 minutes, 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 six arterial blood gases were taken at baseline and at the end of
the hyperoxia period. Minute ventilation (VI ) increased by 21% and
115% with 30% and 75% isocapnic hyperoxia respectively. 75% O2
without any control on PetCO2 led to a 16% increase in VI, but PetCO2
decreased by 3.6 mmHg (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, VI more than doubling after 30 minutes of 75% O2. If
isocapnia is not maintained, hyperventilation is attenuated by a
decrease in arterial PCO2 (PaCO2). There is a correlation between
hyperoxic and hypercapnic ventilatory responses. Based on data from
the literature we calculated that the Haldane effect seems to be the
major cause of hyperventilation during both isocapnic and
poikilocapnic hyperoxia.
Received 17 April 1995; accepted in final form 4 June 1996.
APS Manuscript Number A421-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96