Respiratory modulation of carotid and aortic body reflex left ventricular inotropic responses in the cat

Abstract

Several studies have demonstrated that the cardiac chronotropic responses to selective stimulation of the carotid body chemoreceptors are respiratory modulated. The reflex bradycardia of vagal origin is greater when the excitatory stimuli are delivered in the expiratory phase of the respiratory cycle than when delivered in the inspiratory phase (Haymet & McCloskey, 1975; see also Spyer, 1990). This is accounted for by the excitability of the cardiac vagal preganglionic motoneurones near the nucleus ambiguus varying with the phase of respiration: they become refractory to incoming excitatory stimuli during the inspiratory phase of the respiratory cycle, the excitability of the neurones returning during expiration. Two neurogenic mechanisms are responsible for this refractoriness: first, activity of the central inspiratory neurones mediated by a cholinergic pathway, and second, increased activity of slowly adapting pulmonary stretch receptors driven by lung inflation (see Spyer, 1990 1. The reflex changes in the inotropic state of the left ventricle, measured as the dPÏdtmax (maximum rate of change of pressure), occurring in response to selective stimulation of the carotid and aortic body chemoreceptors by sodium cyanide, were studied in the cat anaesthetized with a mixture of chloralose and urethane. 2. The animals were artificially ventilated with an open pneumothorax. The heart rate and mean arterial blood pressure were maintained constant. 3. With on-going central respiratory activity, stimulation of the carotid bodies caused an increase in respiratory movements. Variable changes in left ventricular dPÏdtmax occurred, the predominant response being an increase. The mean change was 8·3 ± 2·9 % from a control value of 6850 ± 450 mmHg s¢. Stimulation of the aortic bodies resulted in a smaller increase in respiration or no effect, but a significant increase occurred in left ventricular dPÏdtmax of 19·6 ± 2·9 % from a control value of 6136 ± 228 mmHg s¢. No significant changes in left ventricular end-diastolic pressure occurred in response to stimulation of either group of chemoreceptors. 4. Tests of chemoreceptor stimulations were repeated during temporary suppression of the secondary respiratory mechanisms: the central respiratory drive was suppressed reflexly by electrical stimulation of the central cut ends of both superior laryngeal nerves and lung stretch afferent activity was minimized by stopping artificial respiration. Carotid body stimulation again evoked variable responses, the predominant now being a reduction in left ventricular dPÏdtmax of 3·1 % from a control value of 5720 ± 320 mmHg s¢, which was significantly different to that occurring during on-going spontaneous respiration. Aortic body stimulation caused an increase in left ventricular dPÏdtmax similar to the response during on-going spontaneous respiration. 5. The positive inotropic responses were mediated via the sympathetic nervous system, as indicated by their abolition as a result of intravenous injections of the â_adrenoceptor blocking age...

Oxygenation pattern and compensatory responses to hypoxia and hypercapnia following bilateral carotid body resection in humans

“…2014; Tubek et al . 2016), the CO response to hypoxia in bCBR patients most likely reflects undisturbed functionality of aortic bodies to increase HR and contractility (De Burgh Daly & Jones, 1998) and is in line with the maintained (in comparison to pre‐procedural values) HR slope. We believe that preservation of HR reactiveness to hypoxia cannot be attributed to the activation of pulmonary stretch receptors as ventilatory response to hypoxia in bCBR patients is absent.…”

O2‐sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells

“…1997; Brophy et al . 1999), but their ventilatory significance is dubious because no respiratory response could be demonstrated when the aortic bodies were selectively stimulated and no additional effect on hypoxic ventilatory response was observed after aortic nerve transection in chemodenervated rats (De Daly & Jones, 1998; Martin‐Body et al . 1986).…”

Aortic Body Chemoreceptors Regulate Coronary Blood Flow in Conscious Control and Hypertensive Sheep

“…There is also some inconsistency in the relative roles of the CB and the ABs in modulating ventilation during hypoxia. [7][8][9][10][11][12] Previous studies have shown that stimulation of the ABs using sodium cyanide infused into the aortic arch as well as systemic hypoxia caused hyperventilation even post CB denervation in the dog, 7 indicating that the ABs do play a role in the ventilatory response to hypoxia.…”

“…5,6 Gaseous or chemical stimulation of ABs produces a mild increase in ventilation compared with activation of the CBs in anesthetized animals. 7–12…”

“…5,6 Gaseous or chemical stimulation of ABs produces a mild increase in ventilation compared with activation of the CBs in anesthetized animals. [7][8][9][10][11][12] The CBs have been well studied both in normotensive and hypertensive conditions. [13][14][15] In contrast, the Pen et al Aortic Bodies and Coronary Blood Flow physiological role of the ABs in the healthy state has been relatively under-studied, and its role in hypertension remains unexplored.…”