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2016 DEPARTMENT OF MEDICINE RESEARCH DAY Title of Poster: Spinal dorsal column and vagus nerve stimulation modulate vagal afferent transduction of myocardial ischemia Presenter: Siamak Salavatian Division: Cardiology ☐ Faculty ☒ Fellow ☐ Resident ☐ Post-doc Research Fellow ☐ Graduate Student ☐ Medical Student ☐Other Principal Investigator/Mentor: Dr.Jeffrey Laurence Ardell Co-Investigators: Thematic Poster Category: Neurobiology, Smooth, Striated and Cardiac Muscle Function, Cardiac Conduction Systems and Arrhythmias, Biology of Perception and Pain, Psychoneuroimmunology Abstract Background: Autonomic regulation therapy (ART), including vagus nerve stimulation (VNS) and spinal cord stimulation (SCS), is an emerging therapy in managing heart diseases, doing so by modulating multiple elements of the cardiac neuronal hierarchy. Objective: To determine if ART impacts primary cardiac sensory afferent transduction of myocardial ischemia (MI). Methods: Using extracellular recordings in anesthetized canines, cardiac-related nodose ganglia neurons were identified by their response to epicardial touch, great vessel occlusion (inferior vena cava occlusion and descending aorta) and chemical activation of sensory neurites with epicardial veratridine. Neural responses to 1 min left anterior descending (LAD) coronary artery occlusion (CAO) were then evaluated prior to and following either SCS [T1-T3 spinal level; 50Hz, 90% motor threshold] or cervical VNS [20 Hz; 1.2x threshold]. Cardiac nodose neural activity was also assessed at progressive levels of VNS [2 Hz; 1-8 mA]. Results: 65% of cardiac-related nodose neurons responded to LAD CAO, with activity increasing ~140% (0.33±0.08 to 0.79±0.19 impulses/sec, p=0.001). The neural response to LAD CAO was suppressed by SCS (0.85±0.3 to 0.11±0.4, p=0.03) or VNS (0.74±0.26 to 0.11±0.05, p=0.03). Nodose neural activity increased progressively with VNS current from 1 to 5 mA (0.2±0.1 to 0.69±0.1 impulses/sec, p=0.005) but decreased when VNS current exceeded 5 mA (0.69±0.1 to 0.12±0.08 impulses/sec, p=0.004). Conclusions: LAD CAO activates multi-modal and nociceptive afferent inputs to the central nervous system. VNS and SCS have the capability to obtund this afferent response, likely doing so by modifying the myocyte/nerve interface. Cardiac nodose neurons did not show linear response to progressive VNS, indicating they are not simple relay stations, and these processing capabilities of the nodose include a damping function in response to excessive neural input.