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Updated: Aug 6, 2026
Echocardiographic and Histological Examination of Cardiac Morphology in the Mouse
Published on: October 26, 2017
Effects of methylphenidate (Ritalin) on mammalian myocardial ultrastructure
1Department of Anatomy and Neurobiology, St. Louis University Medical Center, MO 63104, USA.
Abstract:
Previous observations have indicated lamellated ultrastructural lesions in the myocardium of a patient treated with methylphenidate (Ritalin) hydrochloride (MPH). A causal relationship between MPH exposure and these membranous changes was tested in the myocardium of rats and mice. Following injection of varying doses of MPH for different periods, myocardial ultrastructure was examined and lesions were quantified by stereological techniques. Myocardial tissue also was stained using techniques selective for acid phosphatase and for sarcoplasmic reticulum to identify possible pathogenetic mechanisms. MPH induced membrane accumulations and lamellations which were not membrane-bound and did not react for acid phosphatase, but stained positively for sarcoplasmic reticulum. Both lesions were highly focal, surrounded by normal appearing myocardial tissue. Lamellations were evident at the earliest timepoints examined and appeared to occur without lysosomal involvement. Lesions were still apparent 12 weeks after terminating MPH. These data suggest that MPH may have persistent, cumulative effects on the myocardium.
Insights
Methylphenidate (Ritalin) hydrochloride (MPH) exposure caused lamellated lesions in rat and mouse hearts. These cardiac changes were persistent, suggesting cumulative effects of MPH on the myocardium.
Area of Science:
- Cardiovascular pathology
- Pharmacology
- Toxicology
Background:
- Previous observations noted lamellated ultrastructural lesions in the myocardium of a patient treated with methylphenidate hydrochloride (MPH).
- A potential causal link between MPH exposure and these cardiac membranous changes required investigation.
Purpose of the Study:
- To determine if methylphenidate hydrochloride (MPH) causes myocardial lesions.
- To investigate the pathogenetic mechanisms and persistence of MPH-induced cardiac changes.
Main Methods:
- Rats and mice were injected with varying doses of MPH for different durations.
- Myocardial ultrastructure was examined, and lesions were quantified using stereological techniques.
- Myocardial tissue was stained for acid phosphatase and sarcoplasmic reticulum to explore pathogenetic mechanisms.
Main Results:
- MPH induced non-membrane-bound membrane accumulations and lamellations in the myocardium.
- These lesions stained positively for sarcoplasmic reticulum but not for acid phosphatase.
- Lesions were focal, surrounded by normal tissue, and persisted for at least 12 weeks after MPH cessation.
Conclusions:
- Methylphenidate hydrochloride (MPH) induces myocardial lesions characterized by lamellations.
- These lesions appear to involve the sarcoplasmic reticulum and are persistent.
- MPH may exert cumulative and long-lasting effects on the myocardium.
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