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Related Experiment Videos

Pyruvate dehydrogenase influences postischemic heart function

E D Lewandowski1, L T White

  • 1Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston.

Circulation
|April 1, 1995
PubMed
Summary
This summary is machine-generated.

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Activating pyruvate dehydrogenase (PDH) in postischemic hearts improves cardiac function by increasing pyruvate oxidation, not glycolysis. This metabolic intervention enhances mechanical work and contractile recovery in the absence of increased glucose utilization.

Area of Science:

  • Cardiology
  • Biochemistry
  • Metabolic Research

Background:

  • Pyruvate dehydrogenase (PDH) activity is crucial for carbohydrate oxidation in the heart.
  • PDH is largely inactive during early reperfusion of postischemic myocardium, reducing pyruvate oxidation.
  • Reduced pyruvate oxidation in postischemic hearts has been observed using 13C NMR spectroscopy.

Purpose of the Study:

  • To investigate if counteracting depressed pyruvate oxidation enhances contractile recovery in postischemic hearts.
  • To determine if improved cardiac function is linked to increased glycolytic activity or glucose oxidation.
  • To assess the role of PDH in influencing metabolic efficiency and mechanical work of postischemic hearts.

Main Methods:

  • Isolated rabbit hearts were subjected to ischemia and reperfusion.

Related Experiment Videos

  • Perfusion with [3-13C]pyruvate as the sole substrate targeted PDH directly.
  • PDH activation was modulated using dichloroacetate (DCA).
  • Mechanical function, oxygen consumption (MVO2), and bioenergetic states were monitored using NMR spectroscopy.
  • Pyruvate oxidation was assessed by measuring 13C incorporation into metabolites like glutamate and alanine.

    • Main Results:

    • PDH activation with DCA did not affect normal heart performance.
    • Postischemic hearts treated with DCA showed improved mechanical function and contractile recovery.
    • Rate-pressure-product (RPP) significantly increased in DCA-treated hearts compared to untreated controls.
    • Oxygen use per unit work improved with DCA treatment, without altering high-energy phosphate levels.
    • DCA treatment significantly increased pyruvate oxidation, evidenced by elevated 13C enrichment in the glutamate pool, without increasing glycolytic activity.

    Conclusions:

    • Depressed PDH activity in postischemic myocardium contributes to contractile dysfunction.
    • Activating PDH and restoring pyruvate oxidation can reverse contractile dysfunction in isolated hearts.
    • Improved cardiac performance was achieved by enhancing pyruvate oxidation alone, independent of increased glycolysis or glucose oxidation.