ArticleCardiovascular research2008
Ecstasy produces left ventricular dysfunction and oxidative stress in rats.
Article in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Protective effects of vitamin E and quercetin against MDMA-induced cardiac and hematological dysfunction in male wistar rats.Pflugers Archiv : European journal of physiology · 2026Article
- Drug-induced mitochondrial dysfunction and cardiotoxicity.American journal of physiology. Heart and circulatory physiology · 2015Review
- Ecstasy (MDMA) Alters Cardiac Gene Expression and DNA Methylation: Implications for Circadian Rhythm Dysfunction in the Heart.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure.Journal of molecular and cellular cardiology · 2013Article
- Effects of adenosine A2a receptor agonist and antagonist on hippocampal nuclear factor-kB expression preceded by MDMA toxicity.Metabolic brain disease · 2013Article
- Collagen XIV is important for growth and structural integrity of the myocardium.Journal of molecular and cellular cardiology · 2012Article
- AT1 receptor-mediated augmentation of angiotensinogen, oxidative stress, and inflammation in ANG II-salt hypertension.American journal of physiology. Renal physiology · 2012Article
- Environmentally persistent free radicals decrease cardiac function before and after ischemia/reperfusion injury in vivo.Journal of receptor and signal transduction research · 2011Article
- Troponin T isoforms and posttranscriptional modifications: Evolution, regulation and function.Archives of biochemistry and biophysics · 2011Review
- Early heart failure in the SMNDelta7 model of spinal muscular atrophy and correction by postnatal scAAV9-SMN delivery.Human molecular genetics · 2010Article
- Oxidative stress contributes to methamphetamine-induced left ventricular dysfunction.Cardiovascular research · 2010Article
- 3,4-Methylenedioxymethamphetamine alters left ventricular function and activates nuclear factor-Kappa B (NF-κB) in a time and dose dependent manner.International journal of molecular sciences · 2010Article
- Metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes.Cardiovascular toxicology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
aimsOur aim was to determine whether the repeated, binge administration of 3,4-methylenedioxymethamphetamine (ecstasy; MDMA) produces structural and/or functional changes in the myocardium that are associated with oxidative stress. METHODS AND
resultsEchocardiography and pressure-volume conductance catheters were used to assess left ventricular (LV) structure and function in rats subjected to four ecstasy binges (9 mg/kg i.v. for 4 days, separated by a 10 day drug-free period). Hearts from treated and control rats were used for either biochemical and proteomic analysis or the isolation of adult LV myocytes. After the fourth binge, treated hearts showed eccentric LV dilation and diastolic dysfunction. Systolic function was not altered in vivo; however, the magnitude of the contractile responses to electrical stimulation was significantly smaller in myocytes from rats treated in vivo with ecstasy compared with myocytes from control rats. The magnitude of the peak increase in intracellular calcium (measured by Fura-2) was also significantly smaller in myocytes from ecstasy-treated vs. control rats. The relaxation kinetics of the intracellular calcium transients were significantly longer in myocytes from ecstasy-treated rats. Ecstasy significantly increased nitrotyrosine content in the left ventricle. Proteomic analysis revealed increased nitration of contractile proteins (troponin-T, tropomyosin alpha-1 chain, myosin light polypeptide, and myosin regulatory light chain), mitochondrial proteins (Ub-cytochrome-c reductase and ATP synthase), and sarcoplasmic reticulum calcium ATPase.
conclusionThe repeated binge administration of ecstasy produces eccentric LV dilation and dysfunction that is accompanied by oxidative stress. These functional responses may result from the redox modification of proteins involved in excitation-contraction coupling and/or mitochondrial energy production. Together, these results indicate that ecstasy has the potential to produce serious cardiac toxicity and ventricular dysfunction.
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Registered trials
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.