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Related Experiment Videos

Preserved left ventricular structure and function in mice with cardiac sympathetic hyperinnervation.

Helen Kiriazis1, Xiao-Jun Du, Xinheng Feng

  • 1Experimental Cardiology Laboratory, Baker Heart Research Institute, P.O. Box 6492 St. Kilda Road Central, Melbourne, Victoria 8008, Australia.

American Journal of Physiology. Heart and Circulatory Physiology
|May 17, 2005
PubMed
Summary

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Cardiac nerve growth factor (NGF) overexpression causes sympathetic hyperinnervation but preserves left ventricular function. Enhanced norepinephrine uptake in the heart likely prevents adverse effects from increased sympathetic stimulation.

Area of Science:

  • Cardiovascular Physiology
  • Neurobiology
  • Molecular Cardiology

Background:

  • Cardiac-specific overexpression of nerve growth factor (NGF) can lead to sympathetic hyperinnervation.
  • While increased sympathetic stimulation may cause adverse cardiac effects, NGF also enhances norepinephrine uptake.
  • The net impact of cardiac NGF on heart function requires investigation.

Purpose of the Study:

  • To investigate the functional consequences of cardiac nerve growth factor (NGF) overexpression.
  • To determine if sympathetic hyperinnervation induced by NGF impacts left ventricular performance.
  • To explore the role of norepinephrine uptake in mediating NGF's effects on the heart.

Main Methods:

  • Echocardiography and invasive catheterization in transgenic (TG) mice overexpressing cardiac NGF and wild-type (WT) littermates.

Related Experiment Videos

  • Histological analysis and catecholamine assays to assess cardiac structure and neurotransmitter levels.
  • Measurement of left ventricular (LV) function, including fractional shortening and +/-dP/dt, with and without isoproterenol stimulation.

    • Main Results:

    • TG mice exhibited significant right ventricular hypertrophy but only mild left ventricular changes.
    • Left ventricular function (fractional shortening, fractional area change, +/-dP/dt) was preserved in TG mice compared to WT.
    • Despite increased norepinephrine in TG LV tissue, elevated plasma dihydroxyphenylglycol and enhanced neuronal uptake suggest increased norepinephrine clearance.

    Conclusions:

    • Cardiac-specific NGF overexpression induces sympathetic hyperinnervation without detrimental effects on left ventricular performance.
    • Enhanced neuronal norepinephrine uptake appears to mitigate potential adverse outcomes associated with increased cardiac sympathetic activity.
    • NGF's dual role in promoting innervation and facilitating norepinephrine uptake influences cardiac function.