ArticleFrontiers in cardiovascular medicine2015
Central Sympathetic Activation and Arrhythmogenesis during Acute Myocardial Infarction: Modulating Effects of Endothelin-B Receptors.
Article in Frontiers in cardiovascular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Beta-blockers and Short-Term Cardiovascular Outcomes In Patients Hospitalized For Acute Coronary Syndrome and a Left Ventricular Ejection Fraction ≥40.Scientific reports · 2020Trial
- Modifications of long-term heart rate variability produced in an experimental model of diet-induced metabolic syndrome.Interface focus · 2023Article
- Endothelin System and Ischemia-Induced Ventricular Tachyarrhythmias.Life (Basel, Switzerland) · 2022Review
- Referred Somatic Hyperalgesia Mediates Cardiac Regulation by the Activation of Sympathetic Nerves in a Rat Model of Myocardial Ischemia.Neuroscience bulletin · 2022Article
- New insights into the central sympathetic hyperactivity post-myocardial infarction: Roles of METTL3-mediated mJournal of cellular and molecular medicine · 2022Article
- Autonomic function and ventricular tachyarrhythmias during acute myocardial infarction.World journal of experimental medicine · 2018Article
- Local conduction during acute myocardial infarction in rats: Interplay between central sympathetic activation and endothelin.Journal of arrhythmia · 2017Article
- Correlation of Ventricular Arrhythmogenesis with Neuronal Remodeling of Cardiac Postganglionic Parasympathetic Neurons in the Late Stage of Heart Failure after Myocardial Infarction.Frontiers in neuroscience · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sympathetic activation during acute myocardial infarction (MI) is an important arrhythmogenic mechanism, but the role of central autonomic inputs and their modulating factors remain unclear. Using the in vivo rat-model, we examined the effects of clonidine, a centrally acting sympatholytic agent, in the presence or absence of myocardial endothelin-B (ETB) receptors. We studied wild-type (n = 20) and ETB-deficient rats (n = 20) after permanent coronary ligation, with or without pretreatment with clonidine. Cardiac rhythm was continuously recorded for 24 h by implantable telemetry devices, coupled by the assessment of autonomic and heart failure indices. Sympathetic activation and arrhythmogenesis were more prominent in ETB-deficient rats during the early phase post-ligation. Clonidine improved these outcomes throughout the observation period in ETB-deficient rats, but only during the delayed phase in wild-type rats. However, this benefit was counterbalanced by atrioventricular conduction abnormalities and by higher incidence of heart failure, the latter particularly evident in ETB-deficient rats. Myocardial ETB-receptors attenuate the arrhythmogenic effects of central sympathetic activation during acute MI. ETB-receptor deficiency potentiates the sympatholytic effects of clonidine and aggravates heart failure. The interaction between endothelin and sympathetic responses during myocardial ischemia/infarction and its impact on arrhythmogenesis and left ventricular dysfunction merits further investigation.
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