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The metabolism of beta-methyl-[1-14C]heptadecanoic acid, a potential myocardial imaging agent, was investigated in perfused hearts and livers from rats. Hepatic uptake is approximately 4.5 times greater than cardiac uptake. In the heart, 66% of beta-methyl-heptadecanoic acid metabolism occurs via omega-oxidation, 33% by esterification and less than 1% via alpha-oxidation. In contrast, 53% of hepatic metabolism of beta-methyl-heptadecanoic acid occurs via alpha-oxidation, 27% via omega-oxidation, and 20% via esterification. Perfusion of hearts and livers with concentrations of beta-methyl-heptadecanoic acid 100 to 1000 times greater than that used for myocardial imaging does not alter any of the physiological and biochemical parameters measured. In the perfused liver, 3-methyl-[1-14C]glutarate was identified as the principal hydrosoluble catabolite of beta-methyl-heptadecanoic acid.
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