Related Experiment Video
Updated: Oct 19, 2025
Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
Chronic exposure to tramadol induces cardiac inflammation and endothelial dysfunction in mice
Marwa H Bakr1, Eman Radwan2,3, Asmaa S Shaltout4
1Department of Histology and Cell Biology, Faculty of Medicine, Assiut University, Assiut, 71515, Egypt. m.elbadawy@aun.edu.eg.
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.
Insights
Prolonged tramadol use damages cardiovascular tissues by increasing oxidative stress and inflammation while decreasing eNOS expression, leading to cardiac toxicity. This study highlights the risks associated with chronic tramadol therapy.
Area of Science:
- Pharmacology
- Cardiovascular Science
- Toxicology
Background:
- Tramadol is a widely prescribed opioid for moderate to severe pain.
- Chronic tramadol use is linked to cardiovascular complications and tissue damage.
- Limited research exists on tramadol's specific cardiovascular effects and mechanisms.
Purpose of the Study:
- To investigate the cardiovascular effects of chronic tramadol exposure.
- To elucidate the underlying mechanisms of tramadol-induced cardiotoxicity.
- To assess the impact on oxidative stress, inflammation, and cardiac function.
Main Methods:
- Mice were administered tramadol hydrochloride (40 mg/kg) orally for four weeks.
- Histopathological alterations in cardiac and aortic tissues were examined.
- Biomarkers for oxidative stress, inflammation, and cardiac damage (LDH, Troponin I, CK-MB) were measured.
- Endothelial nitric oxide synthase (eNOS) expression was evaluated.
Main Results:
- Tramadol exposure caused significant histopathological changes in the heart and aorta.
- Upregulation of oxidative stress and inflammatory markers was observed in cardiac and aortic tissues.
- Tramadol downregulated the expression of eNOS.
- Increased levels of LDH, Troponin I, and CK-MB indicated cardiac damage.
Conclusions:
- Chronic tramadol administration poses risks to the cardiovascular system.
- Tramadol induces cardiotoxicity through oxidative stress, inflammation, and reduced eNOS expression.
- Findings underscore the need for caution in long-term tramadol therapy.
