The heart rate responses to carotid body chemoreceptor stimulation in the cat

MacLeod, Rhona; Scott, Mary J.

doi:10.1113/jphysiol.1964.sp007511

Cited by 35 publications

(36 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Stimulation of the carotid bodies causes slowing of the heart (Bernthal, Greene & Revzin, 1951;Daly & Scott, 1958;Downing, Remensnyder & Mitchell, 1962;MacLeod & Scott, 1964;Scott, 1966a, b) and systemic vasoconstriction (Bernthal, 1938;Daly & Scott, 1962;Daly & Ungar, 1966), whereas excitation of the aortic bodies elicits bradyeardia or tachycardia (Comroe & Mortimer, 1964) and vasoconstriction (Daly, Hazzledine & Howe, 1965;Daly & Ungar, 1966).…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex

James¹,

Daly²

1969

The Journal of Physiology

136

View full text Add to dashboard Cite

SUMMARY1. In the spontaneously breathing anaesthetized dog, the systemic circulation was perfused at constant blood flow; there was no pulmonary blood flow and the systemic arterial blood Po. and PCO, were controlled independently by an extracorporeal isolated pump-perfused donor lung preparation. The carotid and aortic bodies were separately perfused at constant pressure with blood of the same composition as perfused the systemic circulation.2. Apnoeic asphyxia, produced by stopping the recipient animal's lung movements and, at the same time, making the blood perfusing the systemic circulation and the arterial chemoreceptors hypoxic and hypercapnic by reducing the ventilation of the isolated perfused donor lungs, caused an increase in systemic vascular resistance.3. While the systemic arterial blood was still hypoxic and hypercapnic, withdrawal of the carotid and aortic body 'drive' resulted in a striking reduction in systemic vascular resistance. Re-establishing the chemoreceptor 'drive' immediately increased the vascular resistance again.4. Apnoeic asphyxia carried out while the carotid and aortic bodies were continuously perfused with oxygenated blood of normal Pco, had little or no effect on systemic vascular resistance. 5. The systemic vasoconstrictor response produced by apnoeic asphyxia was reduced or abolished by re-establishing the recipient animal's lung movements, and this effect occurred in the absence of changes in the composition of the blood perfusing the systemic circulation and arterial chemoreceptors. This abolition of the vasoconstriction was due to a pulmonary reflex.6. Apnoeic asphyxia slowed the rate of the beating atria due to excita-

show abstract

Section: Introductionmentioning

confidence: 99%

Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex

James¹,

Daly²

1969

The Journal of Physiology

136

View full text Add to dashboard Cite

show abstract

“…This is probably because the magnitude of the hyperventilatory response is greater in the dog for the same secondary effects can be demonstrated in other species if the conditions are carefully managed to maximise their effects. Nevertheless, among the commonly used laboratory animals, both the tachycardia and peripheral vasodilatation secondary to the hyperventilation of selective chemoreceptor stimulation are weak or non-existent in the cat (22,23), a small tachycardia has been recorded in the rabbit (24,25), although whether or not a secondary vasodilatation influence occurs has not been studied. In the rat, a mild secondary tachycardia has been demonstrated, but the vasodilatation is apparently absent (26).…”

Section: Species Differencesmentioning

confidence: 99%

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Jm¹

1998

Braz J Med Biol Res

View full text Add to dashboard Cite

This review describes the ways in which the primary bradycardia and peripheral vasoconstriction evoked by selective stimulation of peripheral chemoreceptors can be modified by the secondary effects of a chemoreceptor-induced increase in ventilation. The evidence that strong stimulation of peripheral chemoreceptors can evoke the behavioural and cardiovascular components of the alerting or defence response which is characteristically evoked by novel or noxious stimuli is considered. The functional significance of all these influences in systemic hypoxia is then discussed with emphasis on the fact that these reflex changes can be overcome by the local effects of hypoxia: central neural hypoxia depresses ventilation, hypoxia acting on the heart causes bradycardia and local hypoxia of skeletal muscle and brain induces vasodilatation. Further, it is proposed that these local influences can become interdependent, so generating a positive feedback loop that may explain sudden infant death syndrome (SIDS). It is also argued that a major contributor to these local influences is adenosine. The role of adenosine in determining the distribution of O 2 in skeletal muscle microcirculation in hypoxia is discussed, together with its possible cellular mechanisms of action. Finally, evidence is presented that in chronic systemic hypoxia, the reflex vasoconstrictor influences of the sympathetic nervous system are reduced and/or the local dilator influences of hypoxia are enhanced. In vitro and in vivo findings suggest this is partly explained by upregulation of nitric oxide (NO) synthesis by the vascular endothelium which facilitates vasodilatation induced by adenosine and other NO-dependent dilators and attenuates noradrenaline-evoked vasoconstriction. Correspondence

show abstract

“…Stimulation of the arterial chemoreceptors evokes bradycardia (and arteriolar vasoconstriction) as a 'primary' reflex response which is best seen when ventilation is kept steady (Daly & Scott, 1958), or halted (McCloskey, 1979). When ventilation is allowed to increase in response to chemoreceptor stimulation, however, tachycardia (and vasodilatation) occur (MacLeod & Scott, 1964;Daly, 1972). Increased breathing, by activating the central and reflex mechanisms outlined above, blocks primary reflex bradycardia (and also, presumably, vasoconstriction: Daly & Robinson, 1968).…”

Section: Introductionmentioning

confidence: 99%

Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Potter¹

1981

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Single and few-fibre cardiac efferent filaments were dissected from the cervical vagus nerve of dogs anaesthetized with chloralose and paralysed with pancuronium.2. Brief selective baroreceptor or chemoreceptor stimuli, given during the expiratory phase ofthe central respiratory cycle and while the lungs were motionless, evoked trains of action potentials in cardiac vagal efferent fibres. These vagal responses outlasted the duration of the stimuli by 1-3 s.3. Briefselective baroreceptororchemoreceptorstimuli given during the inspiratory phase of the central respiratory cycle (monitored as phrenic discharge) but while the lungs were motionless, failed to evoke reflex increases in discharge. Background vagal discharge was also inhibited during central inspiratory activity.4. Brief baroreceptor or chemoreceptor stimuli given during lung inflation but in the expiratory phase of the central respiratory cycle (phrenic silence), also failed to evoke any reflex increase in discharge, but left resting vagal tone relatively unaffected. Only when vagal tone was high was it markedly inhibited by lung inflation, in the absence of central inspiratory activity.5. A point of contrast between the inhibitory effects of lung inflation and of central inspiratory activity is that both tonic and reflexly evoked vagal discharge are inhibited during central inspiratory activity, but lung inflation more markedly inhibits reflexly evoked vagal discharge than tonic vagal discharge. 6. A model is suggested to explain the different mechanisms of inhibition by lung inflation and by central inspiratory activity.

show abstract

The heart rate responses to carotid body chemoreceptor stimulation in the cat

Cited by 35 publications

References 12 publications

Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex

Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

Contact Info

Product

Resources

About