ArticleAmerican journal of respiratory and critical care medicine2012
Carbon monoxide induces cardiac arrhythmia via induction of the late Na+ current.
Article in American journal of respiratory and critical care medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 84 citations in OpenAlex.
- Predictive Role of QTc Prolongation in Carbon Monoxide Poisoning-Related Delayed Neuropsychiatric Sequelae.BioMed research international · 2018Trial
- Heme oxygenase/carbon monoxide system and cardiac conduction system.Medical gas research · 2026Review
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- A comprehensive assessment of carbon monoxide caused mortality via bioinformatics assisted untargeted metabolomics analysis.Forensic science, medicine, and pathology · 2026Article
- Influence of e-cigarettes and their constituents on cardiac rhythm and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2026Review
- S-Nitrosylation in Cardiovascular Disorders: The State of the Art.Biomolecules · 2025Review
- Association of carbon monoxide poisoning with cardiovascular disease risk: A systematic review and meta-analysis.Heliyon · 2024Article
- Inhibition of the voltage-gated potassium channel Kv1.5 by hydrogen sulfide attenuates remodeling through S-nitrosylation-mediated signaling.Communications biology · 2023Article
- Atrial Fibrillation and Silent Coronary Spasm Complicating Severe Carbon Monoxide Poisoning.Cureus · 2023Article
- Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response.Pharmacological reviews · 2022Review
- Antioxidants in Arrhythmia Treatment-Still a Controversy? A Review of Selected Clinical and Laboratory Research.Antioxidants (Basel, Switzerland) · 2022Review
- Homocysteine, Vitamins B6 and Folic Acid in Experimental Models of Myocardial Infarction and Heart Failure-How Strong Is That Link?Biomolecules · 2022Review
- Carbon monoxide releasing molecule-2 suppresses stretch-activated atrial natriuretic peptide secretion by activating large-conductance calcium-activated potassium channels.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Influence of Nicotine from Diverse Delivery Tools on the Autonomic Nervous and Hormonal Systems.Biomedicines · 2022Article
- Carbon monoxide activation of delayed rectifier potassium currents of human cardiac fibroblasts through diverse pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Article
- Mechanistic Insights Into Inflammation-Induced Arrhythmias: A Simulation Study.Frontiers in physiology · 2022Article
- Downregulation of Vascular Hemeoxygenase-1 Leads to Vasculopathy in Systemic Sclerosis.Frontiers in physiology · 2022Article
- Nitrosative Stress and Human Disease: Therapeutic Potential of Denitrosylation.International journal of molecular sciences · 2021Review
- Metabolic changes during carbon monoxide poisoning: An experimental study.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleClinical reports describe life-threatening cardiac arrhythmias after environmental exposure to carbon monoxide (CO) or accidental CO poisoning. Numerous case studies describe disruption of repolarization and prolongation of the QT interval, yet the mechanisms underlying CO-induced arrhythmias are unknown.
objectivesTo understand the cellular basis of CO-induced arrhythmias and to identify an effective therapeutic approach.
methodsPatch-clamp electrophysiology and confocal Ca(2+) and nitric oxide (NO) imaging in isolated ventricular myocytes was performed together with protein S-nitrosylation to investigate the effects of CO at the cellular and molecular levels, whereas telemetry was used to investigate effects of CO on electrocardiogram recordings in vivo. MEASUREMENTS AND MAIN
resultsCO increased the sustained (late) component of the inward Na(+) current, resulting in prolongation of the action potential and the associated intracellular Ca(2+) transient. In more than 50% of myocytes these changes progressed to early after-depolarization-like arrhythmias. CO elevated NO levels in myocytes and caused S-nitrosylation of the Na(+) channel, Na(v)1.5. All proarrhythmic effects of CO were abolished by the NO synthase inhibitor l-NAME, and reversed by ranolazine, an inhibitor of the late Na(+) current. Ranolazine also corrected QT variability and arrhythmias induced by CO in vivo, as monitored by telemetry.
conclusionsOur data indicate that the proarrhythmic effects of CO arise from activation of NO synthase, leading to NO-mediated nitrosylation of Na(V)1.5 and to induction of the late Na(+) current. We also show that the antianginal drug ranolazine can abolish CO-induced early after-depolarizations, highlighting a novel approach to the treatment of CO-induced arrhythmias.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.