ArticlePflugers Archiv : European journal of physiology2015
Changes in the loading conditions induced by vagal stimulation modify the myocardial infarct size through sympathetic-parasympathetic interactions.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 40 citations in OpenAlex.
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- Muscarinic Receptors in Cardioprotection and Vascular Tone Regulation.Physiological research · 2024Review
- Auricular vagus nerve stimulation: a new option to treat inflammation in COVID-19?Revista da Associacao Medica Brasileira (1992) · 2023Article
- The protective effect of vagus nerve stimulation against myocardial ischemia/reperfusion injury: pooled review from preclinical studies.Frontiers in pharmacology · 2023Article
- Auricular vagus nerve stimulator for closed-loop biofeedback-based operation.Analog integrated circuits and signal processing · 2022Article
- Vagus nerve stimulation ameliorates L-NAME-induced preeclampsia-like symptoms in rats through inhibition of the inflammatory response.BMC pregnancy and childbirth · 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
- Tragus Nerve Stimulation Suppresses Post-Infarction Ventricular Arrhythmia by Modulating Autonomic Activity and Heterogeneities of Cardiac Receptor Distribution.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Non-invasive Auricular Vagus Nerve Stimulation as a Potential Treatment for Covid19-Originated Acute Respiratory Distress Syndrome.Frontiers in physiology · 2020Article
- Effects of αβ-Blocker Versus β1-Blocker Treatment on Heart Rate Response During Incremental Cardiopulmonary Exercise in Japanese Male Patients with Subacute Myocardial Infarction.International journal of environmental research and public health · 2019Article
- Current Directions in the Auricular Vagus Nerve Stimulation II - An Engineering Perspective.Frontiers in neuroscience · 2019Review
- Current Directions in the Auricular Vagus Nerve Stimulation I - A Physiological Perspective.Frontiers in neuroscience · 2019Review
- Revisiting the Cardioprotective Effects of Acetylcholine Receptor Activation against Myocardial Ischemia/Reperfusion Injury.International journal of molecular sciences · 2018Review
- Pilocarpine-Induced Status Epilepticus Is Associated with P-Glycoprotein Induction in Cardiomyocytes, Electrocardiographic Changes, and Sudden Death.Pharmaceuticals (Basel, Switzerland) · 2018Article
- Antagonistic and Synergistic Activation of Cardiovascular Vagal and Sympathetic Motor Outflows in Trigeminal Reflexes.Frontiers in neurology · 2017Review
- 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
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a previous research, we described that vagal stimulation increases the infarct size by sympathetic co-activation. The aim of this study was to determine if hemodynamic changes secondary to the vagal stimulation are able to activate sympathetic compensatory neural reflexes, responsible for increasing the infarct size. A second goal was to determine if intermittent vagal stimulation avoids sympathetic activation and reduces infarct size by muscarinic activation of the Akt/glycogen synthase kinase 3 β (GSK-3β) pathway. Rabbits were subjected to 30 min of regional myocardial ischemia and 3 h of reperfusion without vagal stimulation, or the following protocols of right vagus nerve stimulation for 10 min before ischemia: (a) continuous vagal stimulation and (b) intermittent vagal stimulation (cycles of 10 s ON/50 s OFF). Continuous vagal stimulation increased the infarct size (70.7 ± 4.3 %), even after right vagal section (68.6 ± 4.1 %) compared with control group (52.0 ± 3.7 %, p < 0.05). Bilateral vagotomy, pacing, and esmolol abolished the deleterious effect, reaching an infarct size of 43.3 ± 5.1, 43.5 ± 2.1, and 46.0 ± 4.6 % (p < 0.05), respectively. Intermittent stimulation reduced the infarct size to 29.8 ± 3.0 % (p < 0.05 vs I/R). This effect was blocked with atropine (50.2 ± 3.6 %, p < 0.05). Continuous vagal stimulation induced bradycardia and increased the loading conditions and wall stretching of the atria. These changes provoked the co-activation reflex of the sympathetic nervous system, observed by the rise in plasmatic catecholamine levels, which increased the infarct size. Sympathetic co-activation was abolished by continuous vagal stimulation with constant heart rate or parasympathetic deafferentation. Intermittent vagal stimulation attenuated the sympathetic tone and reduced the infarct size by the muscarinic activation of the Akt pathway and GSK-3β inhibition. Continuous stimulation only phosphorylated Akt and GSK-3β when esmolol was administered.
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