ArticleScientific reports2021
Chronic exposure to tramadol induces cardiac inflammation and endothelial dysfunction in mice.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- Modulation of the AMPK/TFEB Axis by Ezetimibe Attenuates Neuroinflammatory, Oxidative Stress, and Neurotransmitter Dysregulation in Naloxone-precipitated Tramadol Withdrawal in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Aurintricarboxylic Acid Attenuates Tramadol Withdrawal Syndrome Via TWEAK/FN14 Inhibition and CREB Modulation in Mice Model.Neuromolecular medicine · 2025Article
- The Influence of Anesthetics on the Functions of the Endothelium and Oxidative Stress: A Critical Review.Biomedicines · 2025Review
- Article
- The toxic profile of tramadol combined with nicotine on the liver and testicles: evidence from endoplasmic reticulum stress.Molecular biology reports · 2023Article
- Potential Impact of 3% Hypertonic Saline Infusion on Tramadol Poisoning-Induced Electrocardiogram Changes; a Randomized Clinical Trial.Archives of academic emergency medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tramadol is an opioid extensively used to treat moderate to severe pain; however, prolonged therapy is associated with several tissues damage. Chronic use of tramadol was linked to increased hospitalizations due to cardiovascular complications. Limited literature has described the effects of tramadol on the cardiovascular system, so we sought to investigate these actions and elucidate the underlying mechanisms. Mice received tramadol hydrochloride (40 mg/kg body weight) orally for 4 successive weeks. Oxidative stress, inflammation, and cardiac toxicity were assessed. In addition, eNOS expression was evaluated. Our results demonstrated marked histopathological alteration in heart and aortic tissues after exposure to tramadol. Tramadol upregulated the expression of oxidative stress and inflammatory markers in mice heart and aorta, whereas downregulated eNOS expression. Tramadol caused cardiac damage shown by the increase in LDH, Troponin I, and CK-MB activities in serum samples. Overall, these results highlight the risks of tramadol on the cardiovascular system.
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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.