Abstract
AimsThe effects of sympatho-vagal interaction on heart rate (HR) changes are characterized by vagal dominance resulting in accentuated antagonism. Complex autonomic modulation of ventricular electrophysiology may exert prognostic arrhythmic impact. We examined the effects of concurrent sympathetic (SNS) and vagus (VNS) nerve stimulation on ventricular fibrillation threshold (VFT) and standard restitution (RT) in an isolated rabbit heart preparation with intact dual autonomic innervation, with and without beta-blockade. Methods and resultsMonophasic action potentials were recorded from left ventricular epicardial surface of dual-innervated isolated heart preparations from New Zealand white rabbits (n = 18). HR, VFT and RT were measured during different stimulation protocols (Protocol 1: VNS-SNS; Protocol 2: SNS-VNS) involving low- and high-frequency stimulations. A sub-study of Protocol 2 was performed in the presence of metoprolol tartrate.In both protocols, HR changes were characterized by vagal-dominant bradycardic component, affirming accentuated antagonism. During concurrent high-frequency VNS (HV), SNS prevails in lowering VFT in a frequency-sensitive manner during low (LS) or high (HS)-frequency stimulations (HV-LS: −2.8 ± 0.8 mA; HV-HS: −4.0 ± 0.9 mA, p < .05 vs. HV), with accompanying steepening of relative RT slope gradients (HV-LS: 223.54 ± 37.41%; HV-HS: 295.20 ± 60.86%, p < .05 vs. HV). In protocol 2, low (LV) and high (HV) vagal stimulations during concurrent HS raised VFT (HS-LV: 1.0 ± 0.4 mA; HS-HV: 3.0 ± 0.6 mA, p < .05 vs HS) with associated flattening of RT slopes (HS-LV: 32.40 ± 4.97%;HS-HV: 38.07 ± 6.37%; p < .05 vs HS). Metoprolol abolished accentuated antagonism in HR changes, reduced VFT and flattened RT globally during SNS-VNS. ConclusionsAccentuated antagonism is absent in ventricular electrophysiological changes during sympatho-vagal interaction with sympathetic effect prevailing, suggesting a different mechanism at the ventricular level from heart rate effects. Metoprolol nullified accentuated antagonism with additional anti-fibrillatory effect beyond adrenergic blockade during sympatho-vagal stimulations.
Highlights
The directionally opposing effects of the activity of the two branches of autonomic nerve system on heart rate (HR) control is well characterized
Effects of background high-frequency vagus nerve stimulation on heart rate response during low and high-frequency sympathetic nerve stimulations In Protocol 1, HR response was first assessed with LS and high-frequency SNS (HS)
Steady-state HR was recorded from atrial electrogram following SNSinduced tachycardia
Summary
The directionally opposing effects of the activity of the two branches of autonomic nerve system on heart rate (HR) control is well characterized. Sympathetic nerve stimulation (SNS) leads to an increase in HR (positive chronotropy) whereas vagus nerve stimulation (VNS) results in a reduction in HR (negative chronotropy) [1] via modulation by catecholamines and acetylcholine respectively on the sino-atrial node [2]. In a dynamic physiological model, sympathetic and vagus nerves exhibit complex interaction with data supporting a vagal dominance in overall HR control during sympatho-vagal interaction [4,5,6,7,8], due to the phenomenon of accentuated antagonism [8]. Accentuated antagonism was observed when the positive chronotropic effect of sympathetic stimulation was attenuated the higher the background vagal tone. The negative chronotropic effect of vagal stimulation was potentiated with increasing sympathetic tone
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