ArticleExperimental physiology2026
Cardioprotection via vagus nerve stimulation preconditioning: Reducing ischaemia-reperfusion injury and arrhythmic risk.
Article in Experimental physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Cardioprotection via vagus nerve stimulation preconditioning: Reducing ischaemia-reperfusion injury and arrhythmic risk.Experimental physiology · 2026Article
- Bidirectional brain-heart communication in coronary heart disease: from coronary plaques to central autonomic networks.Frontiers in neuroscience · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
Acute myocardial infarction is a leading cause of morbidity and mortality, with ischaemia-reperfusion (I/R) injury exacerbating myocardial damage. Vagus nerve stimulation (VNS) has been reported to exert cardioprotective effects, but its efficacy in preconditioning against I/R injury requires further investigation. We evaluated the cardioprotective effects of VNS preconditioning in a rat model of acute myocardial infarction with induced I/R injury. Sixty rats were randomized into Pre-VNS, Control and Sham groups. The Pre-VNS group received 1 week of low-level cervical VNS before induction of I/R injury; stimulation was deactivated 30 min before ischaemia. Survival, echocardiographic function, reperfusion arrhythmias, arrhythmia inducibility, infarct size, apoptosis and inflammatory cytokines were assessed. Survival did not differ significantly between Pre-VNS and Control groups (75.0% vs. 65.0%, p = 0.497). However, Pre-VNS animals exhibited preserved cardiac function, with higher ejection fraction and fractional shortening (p < 0.001). VNS preconditioning reduced the incidence of reperfusion arrhythmia during left anterior descending coronary artery ligature release (p = 0.006) and decreased the arrhythmia index on programmed stimulation (p = 0.003). Infarct size and cardiomyocyte apoptosis were significantly attenuated (p < 0.001), accompanied by markedly lower serum interleukin-1β, interleukin-6 and tumour necrosis factor-alpha levels (p < 0.001). VNS preconditioning effectively mitigates I/R injury by improving cardiac function, reducing infarct size and arrhythmias, and attenuating inflammatory and apoptotic responses.
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Registered trials
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