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Related Experiment Videos

Age-dependent alterations in rat ventricular myocardium: a quantitative analysis.

D L Schmucker, H G Sachs

    Mechanisms of Ageing and Development
    |June 1, 1985
    PubMed
    Summary

    Aging does not degrade cardiac ultrastructure in male Fischer 344 rats. Key cellular components like mitochondria and myofibrils remain stable, with only dense bodies and sarcoplasmic reticulum showing age-related changes.

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    Area of Science:

    • Gerontology
    • Cardiovascular Biology
    • Cellular Ultrastructure

    Background:

    • Cardiac performance declines with age.
    • Age-related ultrastructural changes in the heart are not fully understood.
    • Fischer 344 rats are a common model for aging studies.

    Purpose of the Study:

    • To quantitatively assess age-dependent ultrastructural changes in rat ventricular myocardium.
    • To correlate ultrastructural findings with cardiac aging.
    • To investigate the role of cellular components in age-related cardiac dysfunction.

    Main Methods:

    • Quantitative electron microscopy of rat ventricular myocardium.
    • Stereological analysis of cellular components (mitochondria, myofibrils, lipid, dense bodies, sarcoplasmic reticulum).

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  • Biochemical analysis of lysosomal enzyme activities (acid phosphatase, beta-glucuronidase).

    • Main Results:

    • Volume fractions of mitochondria, myofibrillar mass, and lipid remained unchanged with age.
    • Dense body volume fraction increased four-fold, and sarcoplasmic reticulum volume increased from 6 to 16 months.
    • Lysosomal enzyme activities showed differential aging responses; neither correlated with dense body changes.

    Conclusions:

    • Age-dependent cardiac aging is not explained by a general degradation of cardiac ultrastructure.
    • Specific ultrastructural changes occur, but major components remain intact.
    • The observed changes in cardiac performance with aging may involve mechanisms beyond simple ultrastructural deterioration.