Effect of epinephrine on myocardial triglyceride and free fatty acid utilization

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Abstract
In the isolated perfused rat heart, palmitate produced a 90% suppression of glucose oxidation which was partially reversed by epinephrine. Epinephrine increased C14O2 production from glucose-U-C14 6-fold in the presence of palmitate and 2-fold in its absence, but did not increase the oxidation of circulating chylomicron tripal-mitin-C14 or palmitate-I-C14. Titratable fatty acid (FFA) uptake was less than the palmitate-C14 uptake with the result that there was an exaggerated decrease in perfusate FFA specific activity. Recovery of chylomicron tripalmitin-C14 and palmitate-I-C14 in myocardial triglyceride doubled, possibly as a result of increased exchange between endogenous triglyceride fatty acid and perfusate FFA. Increased glycerol release indicated that endogenous lipid turnover and utilization were enhanced. Hydrolysis and utilization of circulating triglyceride did not correlate with that predicted from studies of myocardial lipoprotein lipase. These experiments suggest that epinephrine: specifically stimulates glucose utilization; increases the utilization of endogenous lipid; indirectly influences myocardial FFA uptake in the intact animal by virtue of its ability to elevate circulating levels of FFA rather than by a direct effect on myocardial extraction.