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Human and canine ventricular vasoactive intestinal polypeptide: decrease with heart failure.

D V Unverferth, T M O'Dorisio, M M Miller

    The Journal of Laboratory and Clinical Medicine
    |July 1, 1986
    PubMed
    Summary
    This summary is machine-generated.

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    Vasoactive intestinal polypeptide (VIP) levels significantly decrease in canine models of heart failure and in human hearts with advanced disease. This suggests VIP may play a role in cardiac function and failure.

    Area of Science:

    • Cardiology
    • Molecular Biology
    • Biochemistry

    Background:

    • Vasoactive intestinal polypeptide (VIP) is a known vasodilator with potential positive inotropic effects.
    • Alterations in VIP levels may be associated with cardiac dysfunction and heart failure.

    Purpose of the Study:

    • To investigate myocardial levels of VIP in experimental models of heart failure.
    • To compare VIP concentrations in human hearts with and without heart failure, considering underlying conditions like coronary artery disease.

    Main Methods:

    • Induction of cardiomyopathy in dogs using cobalt and doxorubicin to measure myocardial VIP levels via radioimmunoassay.
    • Assay of VIP content in left ventricular muscle and papillary muscles from human hearts of transplant recipients and valve replacement patients.

    Related Experiment Videos

  • Measurement of myocardial catecholamines and correlation with VIP levels.
  • Main Results:

    • Myocardial VIP levels decreased significantly in canine models of cobalt-induced and doxorubicin-induced heart failure.
    • Human hearts with advanced heart failure, particularly those with coronary artery disease, exhibited the lowest myocardial VIP concentrations.
    • VIP levels were significantly lower in failing hearts compared to non-failing hearts, with a weak positive correlation noted between VIP and norepinephrine.

    Conclusions:

    • Myocardial VIP levels are reduced in experimental and human heart failure.
    • VIP deficiency may contribute to the pathophysiology of heart failure, especially in the presence of coronary artery disease.
    • Further research is warranted to explore the therapeutic potential of VIP in managing heart failure.