ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016
Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. 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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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Methylene Blue Mitigates Doxorubicin-Induced Cardiotoxicity via KEAP1/NRF2/GPX-4/Caspase3 Modulation.International journal of molecular sciences · 2025Article
- Redirecting Intermediary Metabolism to Counteract Cyanide Poisoning.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Neurological Sequelae of Acute Hydrogen Sulfide Poisoning: A Literature Review, Controversies, and Knowledge Gaps.Neurology international · 2025Review
- Cardiotoxic and Cardioprotective Effects of Methylene Blue in the Animal Model of Cardiac Ischemia and Reperfusion.Biomedicines · 2024Article
- Hydrogen sulfide responsive nanoplatforms: Novel gas responsive drug delivery carriers for biomedical applications.Asian journal of pharmaceutical sciences · 2024Review
- A Sulfonyl Azide-Based Sulfide Scavenger Rescues Mice from Lethal Hydrogen Sulfide Intoxication.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- An Updated Insight Into Molecular Mechanism of Hydrogen Sulfide in Cardiomyopathy and Myocardial Ischemia/Reperfusion Injury Under Diabetes.Frontiers in pharmacology · 2021Review
- Antidotal effects of methylene blue against cyanide neurological toxicity: in vivo and in vitro studies.Annals of the New York Academy of Sciences · 2020Article
- Azure B as a novel cyanide antidote: Preclinical in-vivo studies.Toxicology reports · 2020Article
- Hydrogen Sulfide Toxicity: Mechanism of Action, Clinical Presentation, and Countermeasure Development.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2019Review
- Antidotal Effects of the Phenothiazine Chromophore Methylene Blue Following Cyanide Intoxication.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Article
- Methylene Blue Administration During and After Life-Threatening Intoxication by Hydrogen Sulfide: Efficacy Studies in Adult Sheep and Mechanisms of Action.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Methylene Blue Counteracts HCardiovascular toxicology · 2018Article
- On the Efficacy of Cardio-Pulmonary Resuscitation and Epinephrine Following Cyanide- and HCardiovascular toxicology · 2018Article
- Revisiting the physiological effects of methylene blue as a treatment of cyanide intoxication.Clinical toxicology (Philadelphia, Pa.) · 2018Article
- Methylene blue counteracts cyanide cardiotoxicity: cellular mechanisms.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Analysis of decreases in systemic arterial pressure and heart rate in response to the hydrogen sulfide donor sodium sulfide.American journal of physiology. Heart and circulatory physiology · 2017Article
- H2S concentrations in the heart after acute H2S administration: methodological and physiological considerations.American journal of physiology. Heart and circulatory physiology · 2016Article
- Is exogenous hydrogen sulfide a relevant tool to address physiological questions on hydrogen sulfide?Respiratory physiology & neurobiology · 2016Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously reported that methylene blue (MB) can counteract hydrogen sulfide (H2S) intoxication-induced circulatory failure. Because of the multifarious effects of high concentrations of H2S on cardiac function, as well as the numerous properties of MB, the nature of this interaction, if any, remains uncertain. The aim of this study was to clarify 1) the effects of MB on H2S-induced cardiac toxicity and 2) whether L-type Ca(2+) channels, one of the targets of H2S, could transduce some of the counteracting effects of MB. In sedated rats, H2S infused at a rate that would be lethal within 5 min (24 μM·kg(-1)·min(-1)), produced a rapid fall in left ventricle ejection fraction, determined by echocardiography, leading to a pulseless electrical activity. Blood concentrations of gaseous H2S reached 7.09 ± 3.53 μM when cardiac contractility started to decrease. Two to three injections of MB (4 mg/kg) transiently restored cardiac contractility, blood pressure, and V̇o2, allowing the animals to stay alive until the end of H2S infusion. MB also delayed PEA by several minutes following H2S-induced coma and shock in unsedated rats. Applying a solution containing lethal levels of H2S (100 μM) on isolated mouse cardiomyocytes significantly reduced cell contractility, intracellular calcium concentration ([Ca(2+)]i) transient amplitudes, and L-type Ca(2+) currents (ICa) within 3 min of exposure. MB (20 mg/l) restored the cardiomyocyte function, ([Ca(2+)]i) transient, and ICa The present results offer a new approach for counteracting H2S toxicity and potentially other conditions associated with acute inhibition of L-type Ca(2+) channels.
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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.