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[Changes in the myocardium damaged by strophanthin].

N G Fedosenko, P G Klering, A I Krasovitskiĭ

    Arkhiv Anatomii, Gistologii I Embriologii
    |May 1, 1989
    PubMed
    Summary

    Strophanthin intoxication damages rat heart cells, affecting mitochondria and muscle structure. Adenosine triphosphate (ATP) offers partial protection, but adenosine monophosphate may provide greater therapeutic benefits.

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    Area of Science:

    • Cardiovascular toxicology
    • Cellular biology
    • Biochemistry

    Context:

    • Strophanthin is a cardiac glycoside known for its toxicity.
    • Understanding its mechanism of action at the cellular level is crucial for potential therapeutic interventions.
    • Myocardial tissue in white rats serves as the model system.

    Purpose:

    • To elucidate the cellular and subcellular mechanisms of strophanthin-induced cardiotoxicity.
    • To investigate the protective effects of adenosine triphosphate (ATP) and adenosine monophosphate (AMP) against strophanthin toxicity.
    • To assess histochemical changes in key cardiac enzymes and coenzymes.

    Summary:

    • Strophanthin intoxication in rat myocardium alters mitochondrial morphology (area, perimeter, form factor), increases damaged mitochondrial membrane ratios, and affects sarcoplasmic reticulum and T-system areas.
    • Ultrastructural changes include alterations in myofilaments, Z-lines, and sarcomere length.
    • Histochemical analysis revealed changes in succinate dehydrogenase, lactate dehydrogenase, and nicotinamide coenzyme activity.
    • Adenosine triphosphate (ATP) partially mitigates these ultrastructural and histochemical disturbances.
    • Adenosine monophosphate (AMP) is hypothesized to offer superior therapeutic effects due to its cell membrane permeability.

    Impact:

    • Provides detailed insights into the cellular pathology of strophanthin cardiotoxicity.
    • Highlights the potential of nucleotide-based therapies, specifically AMP, for managing strophanthin poisoning.
    • Contributes to the understanding of cardiac energy metabolism and drug-induced cellular damage.

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