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THE CARDIAC OUTPUT DURING THE STEADY‐STATE IN OXYGEN LACK IN THE UNANÆSTHETIZED RABBIT AND ITS RELATION TO THE EARLY CIRCULATORY RESPONSE
Author(s) -
Korner P. I.,
Edwards A. W. T.
Publication year - 1960
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1960.sp001451
Subject(s) - bradycardia , cardiac output , heart rate , anesthesia , hypoxia (environmental) , tachycardia , circulatory system , medicine , blood pressure , reflex bradycardia , cardiology , mean circulatory filling pressure , ventilation (architecture) , oxygen , chemistry , central venous pressure , mechanical engineering , organic chemistry , engineering
The effects of breathing 11·5 per cent and 10 per cent O 2 for 1 hr. were studied in unanæsthetized rabbits. With 11·5 per cent O 2 there was a large increase in ventilation and the arterial O 2 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 O 2 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 O 2 saturation above about 80 per cent and there was no change in cardiac output. In others with lower arterial O 2 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 pO 2 by inducing tissue hypoxia with carbon monoxide. Reduction of the arterial pO 2 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.