ArticleBasic research in cardiology2015
Vagal nerve stimulation started just prior to reperfusion limits infarct size and no-reflow.
Article in Basic research in cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research Progress of Electrical Stimulation in Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2021Pooled it
- Time course of early and delayed myocardial protection induced by vagal nerve stimulation preconditioning.Basic research in cardiology · 2026Article
- A Review of Vagus Nerve Stimulation for Disease: Comprehensive Theory and Evidence for Mechanisms of Action.Comprehensive physiology · 2026Review
- Microvascular Occlusion and Postrecanalization Hyperperfusion in a Swine Model of Acute Ischemic Stroke.Journal of the American Heart Association · 2025Article
- Review
- Activation of the nonneuronal cholinergic cardiac system by hypoxic preconditioning protects isolated adult cardiomyocytes from hypoxia/reoxygenation injury.American journal of physiology. Heart and circulatory physiology · 2024Article
- Defective recovery of QT dispersion due to no-reflow following acute interventional therapy in patients with ST-segment elevation myocardial infarction.Cardiovascular diagnosis and therapy · 2024Article
- Review
- No robust reduction of infarct size and no-reflow by metoprolol pretreatment in adult Göttingen minipigs.Basic research in cardiology · 2023Article
- Device-Based Approaches Targeting Cardioprotection in Myocardial Infarction: The Expanding Armamentarium of Innovative Strategies.Journal of the American Heart Association · 2022Review
- Closed-Loop Vagus Nerve Stimulation for the Treatment of Cardiovascular Diseases: State of the Art and Future Directions.Frontiers in cardiovascular medicine · 2022Review
- Topical Neck Cooling Without Systemic Hypothermia Attenuates Myocardial Ischemic Injury and Post-ischemic Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
- Chronic Limb Remote Ischemic Conditioning may have an Antihypertensive Effect in Patients with Hypertension.Aging and disease · 2021Review
- Vagus Nerve Stimulation with Mild Stimulation Intensity Exerts Anti-Inflammatory and Neuroprotective Effects in Parkinson's Disease Model Rats.Biomedicines · 2021Article
- Preclinical trial of a MAP4K4 inhibitor to reduce infarct size in the pig: does cardioprotection in human stem cell-derived myocytes predict success in large mammals?Basic research in cardiology · 2021Article
- Myocardial salvage is increased after sympathetic renal denervation in a pig model of acute infarction.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Article
- Cholinergic receptors play a role in the cardioprotective effects of anesthetic preconditioning: Roles of nitric oxide and the CaMKKβ/AMPK pathway.Experimental and therapeutic medicine · 2021Article
- Microbiota, a New Playground for the Omega-3 Polyunsaturated Fatty Acids in Cardiovascular Diseases.Marine drugs · 2021Review
- Myocardial ischaemia-reperfusion injury and cardioprotection in perspective.Nature reviews. Cardiology · 2020Review
- Pathophysiology and diagnosis of coronary microvascular dysfunction in ST-elevation myocardial infarction.Cardiovascular research · 2020Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vagal nerve stimulation (VNS) started prior to, or during, ischemia has been shown to reduce infarct size. Here, we investigated the effect of VNS when started just prior to, and continued during early, reperfusion on infarct size and no-reflow and studied the underlying mechanisms. For this purpose, swine (13 VNS, 10 sham) underwent 45 min mid-LAD occlusion followed by 120 min of reperfusion. VNS was started 5 min prior to reperfusion and continued until 15 min of reperfusion. Area at risk, area of no-reflow (% of infarct area) and infarct size (% of area at risk), circulating cytokines, and regional myocardial leukocyte influx were assessed after 120 min of reperfusion. VNS significantly reduced infarct size from 67 ± 2 % in sham to 54 ± 5 % and area of no-reflow from 54 ± 6 % in sham to 32 ± 6 %. These effects were accompanied by reductions in neutrophil (~40 %) and macrophage (~60 %) infiltration in the infarct area (all p < 0.05), whereas systemic circulating plasma levels of TNFα and IL6 were not affected. The degree of cardioprotection could not be explained by the VNS-induced bradycardia or the VNS-induced decrease in the double product of heart rate and left ventricular systolic pressure. In the presence of NO-synthase inhibitor LNNA, VNS no longer attenuated infarct size and area of no-reflow, which was paralleled by similarly unaffected regional leukocyte infiltration. In conclusion, VNS is a promising novel adjunctive therapy that limits reperfusion injury in a large animal model of acute myocardial infarction.
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