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Coronary hyperperfusion and myocardial metabolism in isolated and intact hearts
W P Miller1, N Shimamoto, S H Nellis
1Section of Cardiology, University of Wisconsin Medical School, Madison 53792.
Insights
Coronary hyperperfusion did not independently increase myocardial oxygen consumption (VO2) in isolated rat hearts or intact swine hearts. Adjusting left ventricular (LV) volume, rather than just increasing coronary blood flow, influenced VO2.
Area of Science:
- Cardiovascular Physiology
- Myocardial Metabolism
- Hemodynamics
Background:
- Coronary blood flow regulation is crucial for meeting myocardial oxygen demands.
- Understanding the direct impact of coronary perfusion pressure on heart metabolism is essential.
Purpose of the Study:
- To determine if coronary hyperperfusion independently affects myocardial metabolism.
- To investigate the relationship between coronary perfusion pressure and myocardial oxygen consumption (VO2).
Main Methods:
- Isolated blood-perfused rat hearts were used with controlled left ventricular (LV) pressures and varying coronary perfusion pressures.
- Intact working swine hearts with fixed cardiac output were studied to assess fatty acid utilization and VO2 under hyperperfusion.
- Radioactive palmitate ([14C(U)]palmitate) was used to measure fatty acid oxidation in swine hearts.
Main Results:
- In rat hearts, increasing coronary perfusion pressure elevated LV pressure and dP/dt, but VO2 only increased when LV volume was fixed.
- In swine hearts, a 70% increase in coronary blood flow due to hyperperfusion did not significantly alter global LV function, VO2, or fatty acid utilization.
- LV volume adjustments, not solely coronary hyperperfusion, were linked to changes in myocardial VO2 in rat models.
Conclusions:
- Coronary hyperperfusion alone is not an independent stimulus for increased myocardial oxygen consumption.
- Myocardial metabolism is influenced by factors beyond coronary blood flow, including ventricular loading conditions.
- These findings highlight the complex interplay between hemodynamics and myocardial energetics.
Abstract:
We determined the independent influence of coronary hyperperfusion on myocardial metabolism in isolated and intact hearts. In an isovolumic blood-perfused rat heart preparation working against a left ventricular (LV) balloon, the effect of increasing coronary perfusion pressure from 100 to 150 mmHg was assessed. In three groups of rat hearts LV volume was fixed to obtain LV peak pressures of 42 +/- 3, 101 +/- 5, and 130 +/- 6 mmHg. With coronary hyperperfusion, LV pressure increased 27, 18, and 16%, LV maximum time derivative of pressure (dP/dt) increased 39, 20, and 22%, and myocardial O2 consumption (VO2) increased 16, 17, and 33%, respectively. In a fourth group, LV peak pressure was held constant at 92 +/- 4 mmHg during coronary hyperperfusion by decreasing LV volume. In this group, despite an increase in coronary blood flow of 48%, there was no significant difference in LV maximum dP/dt or myocardial VO2. Thus, in isolated rat hearts, coronary hyperperfusion was not an independent stimulus to myocardial VO2. To further test this, the effect of coronary hyperperfusion on myocardial metabolism was studied in an intact working swine heart preparation where the cardiac output was fixed with a right heart bypass circuit. Fatty acid oxidation in the left anterior descending bed was assessed by production of 14CO2 from [14C(U)]palmitate. A comparison of coronary perfusion 106 +/- 5 vs. 197 +/- 5 mmHg resulted in no significant change in global LV function, including LV internal diameter. Despite a 70% increase in coronary blood flow, there was no significant change in myocardial VO2 or fatty acid utilization.(ABSTRACT TRUNCATED AT 250 WORDS)