The Cardiac Output of the Unanæsthetized Rabbit, and the Effects of Preliminary Anæsthesia, Environmental Temperature and Carotid Occlusion

Edwards, A. W. T.; Pi, Korner; Thorburn, G. D.

doi:10.1113/expphysiol.1959.sp001403

Cited by 49 publications

(61 citation statements)

References 4 publications

(9 reference statements)

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“…of mean) ml./100 g skin/min. Both values are considerably above the corresponding values in man (Barcroft, 1963;Greenfield, 1963;Shepherd 1963) but have a similar relation to each other and probably reflect the high rate of resting metabolism of the unanaesthetized rabbit (Korner & Darian-Smith, 1954;Edwards et al 1959).…”

Section: Resuiltsmentioning

confidence: 62%

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The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

Chalmers

Korner²,

White³

1966

The Journal of Physiology

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SUMMARY1. The effects of arterial hypoxia on muscle blood flow were examined in normal unanaesthetized rabbits in relation to simultaneously determined changes in cardiac output, arterial pressure and heart rate. Muscle blood flow was estimated from the difference between total limb flow (local thermodilution) and the estimated skin flow (using a calibrated heat conductivity method). The role of the arterial chemoreceptors and baroreceptors in the control of muscle blood flow was examined and the nature of the sympathetic efferent discharge analysed. followed by a return to control values paralleling the changes in cardiac output. In severe arterial hypoxia (Po2 < 30 mm Hg) the initial vasoconstriction was less marked, and during the 'steady state' there was a large vasodilatation and increase in muscle blood flow, at a time when the cardiac output was not elevated.3. The early vasoconstriction in arterial hypoxia is mediated mainly through sympathetic vasoconstrictor nerves as a result of strong arterial chemoreceptor stimulation.4. Increased secretion of adrenaline is an important factor in restoring muscle blood flow to control values during moderate arterial hypoxia, and in elevating the muscle blood flow above these values in severe hypoxia.The peripheral dilator (,8-) effects of adrenaline oppose the peripheral constrictor (a-) effects resulting from increased activation of sympathetic constrictor nerves during arterial hypoxia.

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Section: Resuiltsmentioning

confidence: 62%

“…Gas mixtures were freshly prepared from cylinders of air, N2 and C02, and were administered through a respiratory valve as described previously (Edwards, Korner & Thorburn, 1959). Arterial blood was collected anaerobically, and the pH, P02 and PCO2 determined on 1-5 ml.…”

Section: Introductionmentioning

confidence: 99%

The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

Chalmers

Korner²,

White³

1966

The Journal of Physiology

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“…The operative techniques were carried out under local anaesthesia and included tracheotomy, central ear artery cannulation and right atrial catheterization as described previously [Edwards, Korner and Thorburn, 1959]. Low oxygen mixtures were administered from specially prepared cylinders into a light polythene bag and inspired through the valve system previously described.…”

Section: Methodsmentioning

confidence: 99%

The Immediate‐effects of Acute Hypoxia on the Heart Rate, Arterial Pressure, Cardiac Output and Ventilation of the Unanæsthetized Rabbit

Edwards

1960

Exp Physiol

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The circulatory and respiratory changes occurring during the first 5 min. of hypoxia were studied in unanawsthetized rabbits. Mild degrees of hypoxia produced an increase in ventilation in the rabbit, without eliciting a detectable circulatory response. The early circulatory effects consisted of bradycardia, a rise in mean arterial pressure and a fall in cardiac output, indicating predominant systemic vasoconstriction. The magnitude of the bradyeardia and rise in arterial pressure were related to the fall in arterial 02 saturation. Atropine or vagotomy reduced or abolished the bradycardia, but greatly accentuated the rise in blood pressure. Denervation of the carotid baroreceptors and chemoreceptors almost abolished the bradyeardia and diminished the rise in blood pressure.IN the first few minutes after induction of acute hypoxia most mammalian species develop tachycardia, a moderate rise in mean arterial pressure and an increase in ventilation. It is generally agreed that the role of the arterial chemoreceptors is of paramount importance in the early respiratory drive during oxygen lack [Bjurstedt, 1946;Otis, 1947 and1949]. Up till recently the tachycardia which develops in the early phase of hypoxia has also been considered to be of chemoreceptor origin. Recent observations in dogs on the effects of stimulation of the arterial chemoreceptors by perfusion with venous blood cast considerable doubt on this interpretation, since these procedures usually produce bradyeardia [Bernthal, Greene and Revzin, 1951; Neil, 1956;Scott, 1958 and.The unanaesthetized rabbit develops during the first few minutes of hypoxia a pronounced bradycardia rather than the usual tachyeardia and some rise in arterial pressure. The purpose of this paper is to report the results of an analysis of the mechanism of this early circulatory response to acute hypoxia. METHODSUnanaesthetized rabbits were used in these experiments, except when otherwise stated. The operative techniques were carried out under local anaesthesia and included tracheotomy, central ear artery cannulation and right atrial catheterization

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“…The reason for this was the uncertainty of the adequacy of right atrial sampling in the rabbit, in the estimation of the oxygen content of mixed venous blood. It was shown, however, that the dye and Fick methods compared under these conditions showed good agreement [Edwards, Korner and Thorburn, 1959] and in later experiments the direct Fick method was used for most determinations including controls. In addition to the steady-state observations, continuous recording of arterial blood pressure and heart rate was made from 1-2 min.…”

Section: Methodsmentioning

confidence: 88%

“…The operative procedures consisted of tracheotomy, central ear artery cannulation and right atrial catheterization. Details of these procedures, as well as of the analytical and recording methods used are described elsewhere [Edwards, Korner and Thorburn, 1959;Korner and Edwards, 1959 a]. The gas mixtures used for these experiments varied from 11-5 per cent 02 to 9-8 per cent 02 in N2, and each mixture was given to each animal for 1 hr.…”

Section: Methodsmentioning

confidence: 99%

The Cardiac Output During the Steady‐state in Oxygen Lack in the Unanæsthetized Rabbit and Its Relation to the Early Circulatory Response

Korner

Edwards

1960

Exp Physiol

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The effects of breathing 1-5 per cent and 10 per cent 02 for 1 hr. were studied in unanaesthetized rabbits. With 11-5 per cent 02 there was a large increase in ventilation and the arterial 02 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 02 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., tachyeardia 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 02 saturation above about 80 per cent and there was no change in cardiac output. In others with lower arterial 02 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 P02 by inducing tissue hypoxia with carbon monoxide. Reduction of the arterial P02 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 bypoxia.IN many species acute hypoxia results in an increase in cardiac output. This has been observed regularly with moderate degrees of oxygen lack in man and the unana,sthetized dog [Grollman, 1930; Doyle, Wilson and Warren, 1952;Fishman, McClement, Himmelstein and Cournand, 1952;Nahas, Visscher, Mather, Haddy and Warner, 1954;Asmussen and Nielsen, 1955]. Although most observations have been concerned with steady-state studies, there is evidence in the dog that the cardiac output increases within the first few minutes of hypoxia [Nahas et al., 1954]. It is not known whether the arterial chemoreceptors play a direct part in the elevation of the cardiac output in man and the dog. In contrast to the findings in the dog, the unaneesthetized rabbit develops systemic vasoconstriction during the first few minutes of moderate hypoxia, resulting from intense chemoreceptor

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The Cardiac Output of the Unanæsthetized Rabbit, and the Effects of Preliminary Anæsthesia, Environmental Temperature and Carotid Occlusion

Cited by 49 publications

References 4 publications

The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

The Immediate‐effects of Acute Hypoxia on the Heart Rate, Arterial Pressure, Cardiac Output and Ventilation of the Unanæsthetized Rabbit

The Cardiac Output During the Steady‐state in Oxygen Lack in the Unanæsthetized Rabbit and Its Relation to the Early Circulatory Response

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