Effects of sympatho-vagal interaction on ventricular electrophysiology and their modulation during beta-blockade

Abstract

The 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 results: Monophasic action potentials were recorded from left ventricular epicardial surface of dualinnervated 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:

Autonomic neuro-cardiac profile of electrical, structural and neuronal remodeling in myocardial infarction-induced heart failure

“…In this study, electrophysiologic remodeling in HF was assessed using single autonomic nerve stimulation. We have previously characterized the effects of sympatho-vagal interaction on ventricular electrophysiology of normal hearts, demonstrating the lack of accentuated antagonism (and therefore prevailing sympathetic effect) at the ventricular level [ 10 ]. Instinctively, future studies should assess sympatho-vagal interaction in the in vitro HF model to mimic the complex sympatho-vagal interaction in real life HF population.…”

“…The animal was sacrificed with an overdose of intravenous pentobarbitone sodium (60 mg) and heparin (500 U). Of note, pentobarbitone sodium was chosen due to its inert effect on autonomic function not only in rabbits but other animal models [ [8] , [9] , [10] ]. A 3F polypropylene catheter (Portex, Kent, UK) was inserted through the left ventricular apex for Thebesian venous effluent drainage.…”

“…Using a custom-written program [ 11 ], MAP duration was measured from the beginning of the signal to 90 % repolarization (MAPD 90 ) as described previously ( Supplementary Fig. 2 ) [ 10 ]. A best-fitted exponential curve was calculated (MAPD 90 = MAPD 90max [1-e -DI/Ƭ ]) and fitted using Microcal Origin (v9.1, Origin, San Diego, CA, US) where Ƭ was the time constant.…”

Mechanism of Ventricular Fibrillation: Current Status and Problems

“…Schwartz et al [44] reported that in dogs with a healed anterior wall myocardial infarction, depressed barore ex sensitivity is a powerful indicator for risk strati cation not only after, but even before, the occurrence of a myocardial infarction. Chin et al [45] investigated the effects of sympathetic (SNS) and vagal stimulation (VNS) on VFT and standard restitution in an isolated rabbit heart preparation with and without beta-blockade. During concurrent high-frequency VNS, SNS prevailed in lowering VFT in a frequency-sensitive manner during low-or high-frequency stimulation, with accompanying steepening of relative restitution slope gradients.…”

Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?

“…These agents exert anti-ischemic actions by reducing myocardial metabolic demand and by prolonging diastolic perfusion time secondary to their actions on the sinus node. Moreover, β-blockade obviates action potential changes and increases the threshold for ventricular fibrillation, counterbalancing the pro-fibrillatory effects of myocardial ischemia or sympathetic activation [ 19 ]. Based on these anti-ischemic and anti-arrhythmic properties, β-blockade has been consistently shown to lower SCD rates in post-MI patients.…”