THE CARDIAC OUTPUT DURING THE STEADY-STATE IN OXYGEN LACK IN THE UNANÆSTHETIZED RABBIT AND ITS RELATION TO THE EARLY CIRCULATORY RESPONSE

¹ Cardiopulmonary Research Unit, Department of Physiology, University of Sydney, Sydney, Australia
² Cardiopulmonary Research Unit, Department of Physiology, University of Sydney, Sydney, Australia; Sydney Hospital Fellow in Cardiology

The effects of breathing 11·5 per cent and 10 per cent O₂ for 1 hr. were studied in unanæsthetized rabbits. With 11·5 per cent O₂ there was a large increase in ventilation and the arterial O₂ saturation averaged 86 per cent. There was no significant change in heart rate, arterial pressure or cardiac output after an hour's hypoxia. In animals breathing 10 per cent O₂ the changes in the circulation after 1 hr. correlated well with the severity of bradycardia produced in the first few minutes of hypoxia. This suggested that the circulatory behaviour during the steady-state was related to the activity of the arterial chemoreceptors. In animals in which the early bradycardia was mild there was a relatively small increase in respiratory rate: the cardiac output was increased at the end of 1 hr., tachycardia developed and the blood pressure was either normal or slightly reduced. In other animals the bradycardia and rise in respiratory rate were more marked. Some of these animals maintained an arterial O₂ saturation above about 80 per cent and there was no change in cardiac output. In others with lower arterial O₂ saturations (comparable with those of the high output group) the cardiac output was low at the end of an hour's hypoxia and bradycardia was still present; in this group the early vasoconstriction in the first few minutes of hypoxia seemed to persist.

A high output state was produced in the presence of a normal arterial pO₂ by inducing tissue hypoxia with carbon monoxide. Reduction of the arterial pO₂ superimposed on this state resulted in a fall in cardiac output. It was concluded that the arterial chemoreceptors played no direct part in the development of a high cardiac output in arterial hypoxia.

Note:

We are grateful to Miss Y. Hodgkinson, J. Chalmers and J. Uther for their assistance with the experiments.