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Methods for the Determination of Rates of Glucose and Fatty Acid Oxidation in the Isolated Working Rat Heart
12:24

Methods for the Determination of Rates of Glucose and Fatty Acid Oxidation in the Isolated Working Rat Heart

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Increased nonoxidative glycolysis despite continued fatty acid uptake during demand-induced myocardial ischemia

Margaret P Chandler1, Hazel Huang, Tracy A McElfresh

  • 1Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|April 18, 2002
PubMed

Insights

Coronary artery disease patients under stress experience demand-induced ischemia. This study shows that dobutamine infusion stimulates nonoxidative glycolysis and lactate production without altering myocardial oxygen consumption or fatty acid uptake.

Area of Science:

  • Cardiology
  • Metabolic Physiology
  • Ischemic Heart Disease Research

Background:

  • Patients with coronary artery disease often develop "demand-induced" ischemia during stress.
  • This occurs because they cannot adequately increase coronary blood flow to meet heightened myocardial oxygen demand.

Purpose of the Study:

  • To investigate the metabolic response to demand-induced ischemia.
  • To test if dobutamine infusion with restricted coronary flow stimulates nonoxidative glycolysis without changing myocardial oxygen consumption (MVO(2)) or fatty acid uptake.

Main Methods:

  • Anesthetized open-chest swine hearts (n=7) were used with controlled left anterior descending (LAD) coronary artery flow.
  • Substrate uptake and oxidation were measured using radiotracers during dobutamine infusion and LAD flow reduction.
  • Metabolic changes, including substrate utilization and energy efficiency, were assessed.

Main Results:

  • Despite no change in myocardial oxygen consumption (MVO(2)), there was a significant shift from lactate uptake to production.
  • Glycogen depletion increased by 66%, and glucose uptake rose by 105%.
  • Exogenous fatty acid oxidation decreased by 71%, while fatty acid uptake remained unchanged.

Conclusions:

  • Demand-induced ischemia in this model stimulates nonoxidative glycolysis and lactate production.
  • This metabolic shift occurs without altering myocardial oxygen consumption (MVO(2)) or overall fatty acid uptake.
  • The findings highlight a compensatory metabolic pathway during ischemic stress in coronary artery disease.

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