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Cardiac Sensory Consequences of Low‐Amplitude Autonomic Regulation Therapy
Author(s) -
Ardell Jeffrey L,
Beaumont Eric,
Kenknight Bruce H,
Gibbons David,
Southerland Marie,
Armour John Andrew
Publication year - 2013
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.27.1_supplement.928.10
Subject(s) - medicine , vagus nerve stimulation , vagus nerve , sensory system , nodose ganglion , cardiology , anesthesia , stimulation , spinal cord , neuroscience , biology , psychiatry
Objective To determine if vagus nerve stimulation (VNS) or spinal cord stimulation (SCS) affects the capacity of cardiac afferent neurons to transduce myocardial ischemia (MI). Methods Using extracellular recordings in anesthetized canines, cardiac‐related dorsal root (DRG; T 1 ‐T 3 spinal levels) or nodose ganglia neurons were identified by touch/chemical activation in their epicardial sensory fields located adjacent to the left anterior descending (LAD) coronary artery. Neuronal responses to 1 min LAD coronary artery occlusion (CAO) were then evaluated prior to and following SCS [T1‐T3 spinal level; 50Hz, 90% motor threshold; 20 min] or left cervical VNS [20 Hz; current amplitudes (CA): CA1 (1–1.9 mA) or CA2 (2–3.5 mA); 3 min]. Results LAD CAO activated cardiac afferent neurons in nodose and DRG ganglia, enhancement that persisted for up to 30 min into reperfusion. Following SCS or CA2 VNS, LAD CAO failed to alter their neural activity. VNS at CA1 did not mitigate MI‐induced activation of nodose neurons. Conclusions Transient myocardial ischemia activates primary afferent inputs to the central nervous system (CNS), responses that persist into reperfusion. Pre‐emptive VNS or SCS obtunds sensory transduction of the ischemic myocardium to the CNS, in part accounting for the anti‐anginal and broader cardioprotective effects of such therapy being evaluated clinically. (HL71830)