Effect of epinephrine on myocardial triglyceride and free fatty acid utilization.

$35~$lg. 1966. -In the isolated perfused rat heart, palmitate produced a go% suppression of glucose oxidation which was partially reversed by epinephrine. Epinephrine increased Cl402 production from glucose-U-Cl4 sixfold in the presence of palmitate and twofold in its absence, but did not increase the oxidation of circulating chylomicron tripalmitin-Cl4 or palmitate1 -C l4 Titratable fatty acid (FFA) uptake was less than . the palmitate-Cl4 uptake with the result that there was an exaggerated decrease in perfusate FFA specific activity. Recovery of chylomicron tripalmitin-Cl4 and palmitate-1 -Cl4 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 eninephrine: I) specifically stimulates glucose utilization, 2) increases the utilization of endogenous lipid, and 3) 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.