AJP - Heart and Circulatory Physiology, Vol 253, Issue 5 1271-H1278, Copyright © 1987 by American Physiological Society
Coronary hyperperfusion and myocardial metabolism in isolated and intact hearts
W. P. Miller, N. Shimamoto, S. H. Nellis and A. J. Liedtke
Section of Cardiology, University of Wisconsin Medical School, Madison 53792.
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)
