ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2012
Postconditioning with vagal stimulation attenuates local and systemic inflammatory responses to myocardial ischemia reperfusion injury in rats.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Remodeling of the Intracardiac Ganglia During the Development of Cardiovascular Autonomic Dysfunction in Type 2 Diabetes: Molecular Mechanisms and Therapeutics.International journal of molecular sciences · 2024Review
- Non-invasive vagus nerve stimulation in anti-inflammatory therapy: mechanistic insights and future perspectives.Frontiers in neuroscience · 2024Review
- Magnetic vagus nerve stimulation alleviates myocardial ischemia-reperfusion injury by the inhibition of pyroptosis through the MJournal of nanobiotechnology · 2023Article
- Review
- Vagus Nerve Stimulation and Its Cardioprotective Abilities: A Systematic Review.Journal of clinical medicine · 2023Review
- Transcutaneous auricular vagus nerve stimulation in the treatment of disorders of consciousness: mechanisms and applications.Frontiers in neuroscience · 2023Review
- Neural reflex control of vascular inflammation.Bioelectronic medicine · 2020Review
- Trigger, Signaling Mechanism and End Effector of Cardioprotective Effect of Remote Postconditioning of Heart.Current cardiology reviews · 2019Review
- Modulatory effects of vagal stimulation on neurophysiological parameters and the cellular immune response in the rat brain during systemic inflammation.Intensive care medicine experimental · 2016Article
- Vagus nerve stimulation attenuates myocardial ischemia/reperfusion injury by inhibiting the expression of interleukin-17A.Experimental and therapeutic medicine · 2016Article
- Vagus nerve stimulation mitigates intrinsic cardiac neuronal and adverse myocyte remodeling postmyocardial infarction.American journal of physiology. Heart and circulatory physiology · 2015Article
- Combined Vagal Stimulation and Limb Remote Ischemic Perconditioning Enhances Cardioprotection via an Anti-inflammatory Pathway.Inflammation · 2015Article
- Vagal nerve stimulation started just prior to reperfusion limits infarct size and no-reflow.Basic research in cardiology · 2015Article
- Device-based autonomic modulation in arrhythmia patients: the role of vagal nerve stimulation.Current treatment options in cardiovascular medicine · 2015Article
- Optimal intervention time of vagal stimulation attenuating myocardial ischemia/reperfusion injury in rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
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Authors and funding
8 authors.
Funding
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Abstract
objectiveTo assess effects of postconditioning with the vagal stimulation (VS) on the local and systematic inflammatory responses to acute myocardial ischemia reperfusion injury (IRI).
methodsSixty male Sprague-Dawley rats were randomly allocated into three groups: sham group, ischemia reperfusion group (IR group), and postconditioning with the VS group (POVS group). Serum levels of inflammatory cytokines during reperfusion and myocardial levels of inflammatory cytokines in both ischemic and non-ischemic regions at the end of the experiment were assayed. The infarct size was assessed by Evans blue and triphenyltetrazolium chloride staining.
resultsThe infarct size was significantly reduced in the POVS group compared to the IR group. Serum levels of TNF-α at 30, 60, and 120 min of reperfusion and serum levels of HMGB-1, ICAM-1, IL-1, and IL-6 at 120 min of reperfusion were significantly lower in the POVS group than in the IR group. Myocardial levels of TNF-α, HMGB-1, ICAM-1, IL-1, and IL-6 in both ischemic and non-ischemic regions were also significantly reduced in the POVS group compared with the IR group.
conclusionsPostconditioning with the VS can significantly attenuate the local and systemic inflammatory responses to myocardial IRI, and provide an obvious cardioprotection.
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