ArticleFrontiers in cardiovascular medicine2022
LL-VNS attenuates SK2 expression and incidence of arrhythmias following acute myocardial infarction in rats.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.
- The developments and emerging trends of Autonomic Nervous System Research in Arrhythmia: a bibliometric study from 2004 to 2024.Frontiers in neuroscience · 2025Pooled it
- Cardioprotection via vagus nerve stimulation preconditioning: Reducing ischaemia-reperfusion injury and arrhythmic risk.Experimental physiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Our previous study has demonstrated that low-level vagus nerve stimulation (LL-VNS) protects the heart against ventricular arrhythmias (VAs) induced by acute myocardial infarction (AMI). However, the potential mechanisms by which it influences ventricular electrophysiology remain unknown. Materials and methods: Forty-five rats were divided into three groups: a Control group (sham AMI followed by sham LL-VNS, Results: AMI directly induced hyperactivity in the LSG and reduced vagal tone as indexed by HRV. AMI also decreased VFT, and shortened ERP but increased ERP dispersion. AMI resulted in an increase in expression of ventricular small-conductance Ca Conclusion: LL-VNS altered the electrophysiological properties of the ventricles through inhibition of cardiac sympathetic nervous activity and reduction in SK2 expression.
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Registered trials
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