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Catecholamine-induced myocardial cell damage: catecholamines or adrenochrome.

A M Wheatley, F T Thandroyen, L H Opie

    Journal of Molecular and Cellular Cardiology
    |April 1, 1985
    PubMed
    Summary

    Catecholamine-induced myocardial damage results from direct beta-adrenergic stimulation, not its metabolites. Increased cardiac workload exacerbates this damage, while adrenochrome shows cardiotoxicity only at high, non-physiological concentrations.

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    Area of Science:

    • Cardiology
    • Pharmacology
    • Biochemistry

    Background:

    • Catecholamines, like epinephrine, can cause myocardial damage.
    • The role of catecholamine metabolites, particularly adrenochrome, in this damage is debated.
    • Understanding the mechanism of catecholamine cardiotoxicity is crucial for clinical management.

    Purpose of the Study:

    • To differentiate between direct catecholamine effects and metabolite-induced damage on the heart.
    • To investigate the influence of cardiac workload on catecholamine-mediated myocardial injury.
    • To assess the cardiotoxic potential of physiological and non-physiological catecholamine metabolites.

    Main Methods:

    • Langendorff and left atrial perfused rat heart models were used.
    • Epinephrine and its metabolites (metanephrine, dihydroxymandelic acid, vanillylmandelic acid, adrenochrome) were perfused at varying concentrations.

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  • Lactate dehydrogenase (LDH) release was measured as an indicator of myocardial damage.
  • Beta-adrenoceptor antagonism with atenolol was employed.

    • Main Results:

    • Epinephrine (10^-6 M) significantly increased LDH release, indicating myocardial damage, especially under higher perfusion pressure (100 cm H2O).
    • Beta-1 adrenergic stimulation provoked enzyme leakage, which was prevented by atenolol.
    • Physiological metabolites and adrenochrome (up to 10^-4 M) did not cause significant LDH release.
    • Adrenochrome (10^-4 M) induced contractile failure and coronary vasoconstriction, but only at a concentration deemed pathophysiologically irrelevant.

    Conclusions:

    • Epinephrine-induced myocardial cellular damage is primarily due to direct beta-adrenergic receptor stimulation, not its metabolites.
    • Cardiac workload significantly influences the extent of catecholamine-induced myocardial damage.
    • Adrenochrome is not responsible for catecholamine-induced myocardial cellular damage under physiological conditions.