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Related Experiment Videos

Cardiac sympathetic nerve function in congestive heart failure

G Eisenhofer1, P Friberg, B Rundqvist

  • 1Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-1424, USA. ge@box-h.nih.gov

Circulation
|May 1, 1996
PubMed
Summary

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Congestive heart failure increases norepinephrine release and reduces reuptake efficiency, leading to higher cardiac adrenergic drive. Reduced norepinephrine stores limit turnover despite increased release in failing hearts.

Area of Science:

  • Cardiovascular Physiology
  • Neuropharmacology
  • Heart Failure Pathophysiology

Background:

  • Increased cardiac adrenergic drive and depleted myocardial norepinephrine (NE) stores are implicated in congestive heart failure (CHF) progression.
  • The precise mechanisms underlying these neurochemical abnormalities in CHF require detailed investigation.

Purpose of the Study:

  • To investigate the neurochemical mechanisms of norepinephrine (NE) abnormalities in the failing heart.
  • To assess NE kinetics, storage, and turnover in subjects with and without congestive heart failure.

Main Methods:

  • Intravenous infusion of radiolabeled NE ([3H]NE) in subjects with and without CHF.
  • Measurement of arterial and coronary venous plasma NE and metabolites to assess cardiac NE spillover, reuptake, vesicular exchange, and stores.

Related Experiment Videos

  • Assessment of tyrosine hydroxylase activity and NE turnover.

    • Main Results:

    • Both NE release and reuptake were elevated in failing hearts, but reduced reuptake efficiency led to disproportionately increased NE spillover.
    • Cardiac NE stores were significantly lower (47%) and vesicular leakage of NE was reduced (42%) in CHF.
    • Increased cardiac spillover of dopa and NE turnover were observed in CHF.

    Conclusions:

    • Increased NE release and impaired NE reuptake contribute to heightened cardiac adrenergic drive in CHF.
    • Reduced NE stores in the failing heart limit NE turnover despite increased release.
    • Chronically increased NE turnover and reduced reuptake/storage efficiency, not insufficient tyrosine hydroxylation, likely cause decreased NE stores in CHF.