• Siamak Salavatian, Eric Beaumont, David Gibbons, Matthew Hammer, Donald B Hoover, Armour J Andrew JA UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, United States; UCLA Cardiac Arrhythmia Center, Los Angeles, CA, United States., and Jeffrey L Ardell.
• UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, United States; UCLA Cardiac Arrhythmia Center, Los Angeles, CA, United States.
• Auton Neurosci. 2017 Dec 1; 208: 57-65.

BackgroundAutonomic regulation therapy involving either vagus nerve stimulation (VNS) or spinal cord stimulation (SCS) represents emerging bioelectronic therapies for heart disease. The objective of this study was to determine if VNS and/or SCS modulate primary cardiac afferent sensory transduction of the ischemic myocardium.MethodsUsing extracellular recordings in 19 anesthetized canines, of 88 neurons evaluated, 36 ventricular-related nodose ganglia sensory neurons were identified by their functional activity responses to epicardial touch, chemical activation of their sensory neurites (epicardial veratridine) and great vessel (descending aorta or inferior vena cava) occlusion. Neural responses to 1min left anterior descending (LAD) coronary artery occlusion (CAO) were then evaluated. These interventions were then studied following either: i) SCS [T1-T3 spinal level; 50Hz, 90% motor threshold] or ii) cervical VNS [15-20Hz; 1.2× threshold].ResultsLAD occlusion activated 66% of identified nodose ventricular sensory neurons (0.33±0.08-0.79±0.20Hz; baseline to CAO; p<0.002). Basal activity of cardiac-related nodose neurons was differentially reduced by VNS (0.31±0.11 to 0.05±0.02Hz; p<0.05) as compared to SCS (0.36±0.12 to 0.28±0.14, p=0.59), with their activity response to transient LAD CAO being suppressed by either SCS (0.85±0.39-0.11±0.04Hz; p<0.03) or VNS (0.75±0.27-0.12±0.05Hz; p<0.04). VNS did not alter evoked neural responses of cardiac-related nodose neurons to great vessel occlusion.ConclusionsBoth VNS and SCS obtund ventricular ischemia induced enhancement of nodose afferent neuronal inputs to the medulla.Copyright © 2017 Elsevier B.V. All rights reserved.

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