Activation of the carotid body increases directly recorded cardiac sympathetic nerve activity and coronary blood flow in conscious sheep

Abstract

Activation of the carotid body (CB) using intracarotid potassium cyanide (KCN) injection increases coronary blood flow (CoBF). This increase in CoBF is considered to be mediated by co-activation of both the sympathetic and parasympathetic nerves to the heart. However, whether cardiac sympathetic nerve activity (cardiac SNA) actually increases during CB activation has not been determined previously. We hypothesized that activation of the CB would increase directly recorded cardiac SNA, which would cause coronary vasodilatation. Experiments were conducted in conscious sheep implanted with electrodes to record cardiac SNA and diaphragmatic electromyography (dEMG), flow probes to record CoBF and cardiac output and a catheter to record arterial pressure. Intracarotid KCN injection was used to activate the CB. To eliminate the contribution of metabolic demand on coronary flow, the heart was paced at a constant rate during CB chemoreflex stimulation. Intra-carotid KCN injection resulted in a significant increase in directly recorded cardiac SNA frequency (from 24±2 to 40±4 bursts/minute; p<0.05) as well as a dose-dependent increase in mean arterial pressure (79±15 to 88±14 mmHg; p<0.01) and CoBF (75±37 Vs 86±42 mL/min; p<0.05). The increase in CoBF and coronary vascular conductance to intracarotid KCN injection was abolished after propranolol infusion, suggesting that the increased cardiac SNA mediates coronary vasodilatation. The pressor response to activation of the CB was abolished by pre-treatment with intravenous atropine but there was no change in the coronary flow response. Our results indicate that CB activation increases directly recorded cardiac SNA which mediates vasodilatation of the coronary vasculature.

Regulation of Coronary Blood Flow by the Carotid Body Chemoreceptors in Ovine Heart Failure

“…Previous papers have shown that carotid chemoreflex stimulation by nicotine causes coronary vasodilation in conscious control animals mediated by parasympathetic cholinergic efferent fibers (Hackett et al, 1972;Shen et al, 1994) although this is to contrast to our previous study (Pachen et al, 2020). In our present study, the increased CoBF in both control and HF sheep in response to CB stimulation were unchanged following intravenous atropine infusion.…”

“…(Pachen et al, 2020). Importantly, infusion of the non-selective beta-blocker propranolol abolished the increase in CoBF (Pachen et al, 2020). We concluded that the β2-adrenergic vasodilatory actions supersede the alpha receptor vasoconstriction during reflex sympathetic activation and are responsible for the coronary vasodilatation.…”

“…However, neural control of the coronary artery resistance has also been shown to play an important role. In this context, our previous study in conscious sheep showed that activation of the CB increased directly recorded cardiac SNA and CoBF (Pachen et al, 2020). Importantly when the effects of sympathetic activation was blocked, the increase in CoBF was abolished indicating activation of the chemoreflex increases cardiac SNA which augments CoBF (Pachen et al, 2020).…”

“…*p < 0.05 denotes a significant effect of time (ANOVA, *effect within 1 min time after injections; # significant interaction effect of time × group). (Pachen et al, 2020). Importantly, infusion of the non-selective beta-blocker propranolol abolished the increase in CoBF (Pachen et al, 2020).…”

Model for Identifying High Carotid Body Chemosensitivity in Patients with Obstructive Sleep Apnea

“…CB activation increases sympathetic activity and also simultaneously increases cardiac vagal as well as cardiac sympathetic nerve activity, causing HRV. 33 , 34 OSA patients also have high sympathetic activity, even during normoxic wakefulness. 35 HRV is a common quantitative index for evaluating sympatho-parasympathetic balance, 36 which makes it a promising indicator of CBC.…”