ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Glycolytic inhibition causes spontaneous ventricular fibrillation in aged hearts.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia.Nature cardiovascular research · 2023Article
- The Aging Heart: A Molecular and Clinical Challenge.International journal of molecular sciences · 2022Review
- Antiarrhythmic and Inotropic Effects of Selective NaInternational journal of molecular sciences · 2022Review
- Suppression of ventricular arrhythmias by targeting late L-type Ca2+ current.The Journal of general physiology · 2021Article
- Review
- Role of sodium glucose co-transporter 2 inhibitors in patients with heart failure: an elusive mechanism.Annals of medicine · 2020Review
- Cardiac function and incidence of unexplained myocardial scarring in patients with primary carnitine deficiency - a cardiac magnetic resonance study.Scientific reports · 2019Article
- Effect of myocyte-fibroblast coupling on the onset of pathological dynamics in a model of ventricular tissue.Scientific reports · 2017Article
- Enhanced Late Na and Ca Currents as Effective Antiarrhythmic Drug Targets.Frontiers in pharmacology · 2017Review
- SERCA2a upregulation ameliorates cellular alternans induced by metabolic inhibition.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Relaxin suppresses atrial fibrillation in aged rats by reversing fibrosis and upregulating Na+ channels.Heart rhythm · 2016Article
- Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension.The Journal of physiology · 2016Article
- Synergism between Enhanced Late Inward Currents and Tissue Fibrosis in the Initiation of Spontaneous Ventricular Tachyarrhythmias.Journal of heart health · 2016Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Cardiovascular KPathobiology of aging & age related diseases · 2016Review
- Article
- Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation.Circulation · 2015Article
- Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.Journal of arrhythmia · 2014Article
- Selective Na(+) /Ca(2+) exchanger inhibition prevents Ca(2+) overload-induced triggered arrhythmias.British journal of pharmacology · 2014Article
- New antiarrhythmic targets to control intracellular calcium handling.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Selective glycolytic inhibition (GI) promotes electromechanical alternans and triggered beats in isolated cardiac myocytes. We sought to determine whether GI promotes triggered activity by early afterdepolarization (EAD) or delayed afterdepolarizations in intact hearts isolated from adult and aged rats. Dual voltage and intracellular calcium ion (Ca(i)(2+)) fluorescent optical maps and single cell glass microelectrode recordings were made from the left ventricular (LV) epicardium of isolated Langendorff-perfused adult (∼4 mo) and aged (∼24 mo) rat hearts. GI was induced by replacing glucose with 10 mM pyruvate in oxygenated Tyrode's. Within 20 min, GI slowed Ca(i)(2+) transient decline rate and shortened action potential duration in both groups. These changes were associated with ventricular fibrillation (VF) in the aged hearts (64 out of 66) but not in adult hearts (0 out of 18; P < 0.001). VF was preceded by a transient period of focal ventricular tachycardia caused by EAD-mediated triggered activity leading to VF within seconds. The VF was suppressed by the ATP-sensitive K (K(ATP)) channel blocker glibenclamide (1 μM) but not (0 out of 7) by mitochondrial K(ATP) block. The Ca-calmodulin-dependent protein kinase II (CaMKII) blocker KN-93 (1 μM) prevented GI-mediated VF (P < 0.05). Block of Na-Ca exchanger (NCX) by SEA0400 (2 μM) prevented GI-mediated VF (3 out of 6), provided significant bradycardia did not occur. Aged hearts had significantly greater LV fibrosis and reduced connexin 43 than adult hearts (P < 0.05). We conclude that in aged fibrotic unlike in adult rat hearts, GI promotes EADs, triggered activity, and VF by activation of K(ATP) channels CaMKII and NCX.
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