Metabolic rates in normal and infarcted myocardium.

The effects of myocardial infarction in rat hearts on the utilization of fatty acids and glucose by the surviving, non-infarcted tissue were studied. Hearts were removed from the animals one-week post-infarcted and perfused in the isolated working heart preparation. Oxygen consumption and oxidation of palmitate and glucose were determined at two levels of cardiac work. Rates of substrate oxidation were estimated by 14CO2 production from [14C]-labeled substrates. This approach to measuring metabolic rates may seriously under-estimate the true oxidative rate particularly when measuring oxidation of long-chain fatty acids. Because of the large endogenous stores of fatty acids in tissue lipids, the [14C]-specific activity of the intracellular metabolites involved in the free fatty acids oxidation pathway do not equilibrate with the specific activity of the perfusate fatty acids oxidation pathway do not equilibrate with the specific activity of the perfusate fatty acid even when 14CO2 production has reached an apparent steady state. When comparing an experimental condition to the normal heart, a lower rate of 14CO2 production may not necessarily indicate a lower rate of oxidation of free fatty acids, but a difference in the rate of turnover of endogenous sources of unlabeled fatty acid such that the specific activity of intracellular metabolites equilibrate with extracellular labeled substrate to a lesser extent than in the normal heart. At physiological concentrations of fatty acids, a shift from fatty acid to carbohydrate oxidation occurred in the hypertrophied, surviving tissue following myocardial infarction in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)