ArticleAnesthesiology2023
GABAergic Signaling during Spinal Cord Stimulation Reduces Cardiac Arrhythmias in a Porcine Model.
Article in Anesthesiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- Pulsed Ultrahigh Frequency Spinal Cord Stimulation for Arrhythmia After Myocardial Infarction.Journal of the American Heart Association · 2026Article
- Remote Activation of Spinal TRPV1 by Magnetic Nanocubes Confers Cardioprotection Against Myocardial Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Activation of Spinal Astrocyte α2A Adrenoceptors Protects Against Sepsis-Induced Heart Injury Through Inhibition of GABAergic Neuronal Necroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neuromodulation of the Cardiac Autonomic Nervous System for Arrhythmia Treatment.Biomedicines · 2025Review
- Observational
- Spinal cord stimulation induces Neurotrophin-3 to improve diabetic foot disease.Medical molecular morphology · 2025Article
- Mechanisms and clinical progress of spinal cord stimulation in refractory chronic pain: an overview.Frontiers in neurology · 2025Review
- Improving Sensitivity and Longevity of In Vivo Glutamate Sensors with Electrodeposited NanoPt.ACS applied materials & interfaces · 2024Article
- Modulating the Cardiac Autonomic Nervous System: Stay Close to My Heart or Keep Your Distance?Anesthesiology · 2023Article
- Spinal neuromodulation mitigates myocardial ischemia-induced sympathoexcitation by suppressing the intermediolateral nucleus hyperactivity and spinal neural synchrony.Frontiers in neuroscience · 2023Article
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7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundNeuraxial modulation, including spinal cord stimulation, reduces cardiac sympathoexcitation and ventricular arrhythmogenesis. There is an incomplete understanding of the molecular mechanisms through which spinal cord stimulation modulates cardiospinal neural pathways. The authors hypothesize that spinal cord stimulation reduces myocardial ischemia-reperfusion-induced sympathetic excitation and ventricular arrhythmias through γ-aminobutyric acid (GABA)-mediated pathways in the thoracic spinal cord.
methodsYorkshire pigs were randomized to control (n = 11), ischemia-reperfusion (n = 16), ischemia-reperfusion plus spinal cord stimulation (n = 17), ischemia-reperfusion plus spinal cord stimulation plus γ-aminobutyric acid type A (GABAA) or γ-aminobutyric acid type B (GABAB) receptor antagonist (GABAA, n = 8; GABAB, n = 8), and ischemia-reperfusion plus GABA transaminase inhibitor (GABAculine, n = 8). A four-pole spinal cord stimulation lead was placed epidurally (T1 to T4). GABA modulating pharmacologic agents were administered intrathecally. Spinal cord stimulation at 50 Hz was applied 30 min before ischemia. A 56-electrode epicardial mesh was used for high-resolution electrophysiologic recordings, including activation recovery intervals and ventricular arrhythmia scores. Immunohistochemistry and Western blots were performed to measure GABA receptor expression in the thoracic spinal cord.
resultsCardiac ischemia led to myocardial sympathoexcitation with reduction in activation recovery interval (mean ± SD, -42 ± 11%), which was attenuated by spinal cord stimulation (-21 ± 17%, P = 0.001). GABAA and GABAB receptor antagonists abolished spinal cord stimulation attenuation of sympathoexcitation (GABAA, -9.7 ± 9.7%, P = 0.043 vs. ischemia-reperfusion plus spinal cord stimulation; GABAB, -13 ± 14%, P = 0.012 vs. ischemia-reperfusion plus spinal cord stimulation), while GABAculine alone caused a therapeutic effect similar to spinal cord stimulation (-4.1 ± 3.7%, P = 0.038 vs. ischemia-reperfusion). The ventricular arrhythmia score supported these findings. Spinal cord stimulation during ischemia-reperfusion increased GABAA receptor expression with no change in GABAB receptor expression.
conclusionsThoracic spinal cord stimulation reduces ischemia-reperfusion-induced sympathoexcitation and ventricular arrhythmias through activation of GABA signaling pathways. These data support the hypothesis that spinal cord stimulation-induced release of GABA activates inhibitory interneurons to decrease primary afferent signaling from superficial dorsal horn to sympathetic output neurons in the intermediolateral nucleus. EDITOR’S PERSPECTIVE:
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