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Spinal Dorsal Column and Vagus Nerve Stimulation Modulate Vagal Afferent Transduction of Myocardial Ischemia
Author(s) -
Salavatian Siamak,
Beaumont Eric,
Armour John Andrew,
Ardell Jeffrey L.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.846.13
Subject(s) - medicine , vagus nerve stimulation , vagus nerve , anesthesia , nodose ganglion , cardiology , stimulation , occlusion
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 19 anesthetized canines, 36 cardiac‐related nodose ganglia neurons were identified by their response to epicardial touch, great vessel occlusion (inferior vena cava occlusion and descending aorta), left anterior descending (LAD) coronary artery occlusion(CAO) and chemical activation of sensory neurites with epicardial veratridine. Neural responses to 1 min LAD CAO were then evaluated prior to and following either SCS [T1–T3 spinal level; 50Hz, 90% motor threshold] or cervical VNS [15–20 Hz; 1.2× threshold]. Cardiac nodose neural activity was also assessed at progressive levels of VNS [2 Hz; 1–8 mA]. Results 66% of cardiac‐related nodose neurons responded to LAD CAO, with activity increasing ~140% (0.33±0.08 to 0.79±0.19 Hz, p=0.001). The neural response to LAD CAO was suppressed by SCS (0.85±0.3 to 0.11±0.4 Hz, p=0.03) or VNS (0.74±0.26 to 0.11±0.05 Hz, 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 Hz, p=0.005) but decreased when VNS current exceeded 5 mA (0.69±0.1 to 0.12±0.08 Hz, 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. Support or Funding Information none.