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Research Article Free access | 10.1172/JCI106082
Cardiovascular Division, Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts 02115
Department of Medicine, Cornell University Medical College, New York 10021
Institute for Muscle Disease, Inc., New York 10021
Find articles by Most, A. in: JCI | PubMed | Google Scholar
Cardiovascular Division, Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts 02115
Department of Medicine, Cornell University Medical College, New York 10021
Institute for Muscle Disease, Inc., New York 10021
Find articles by Brachfeld, N. in: JCI | PubMed | Google Scholar
Cardiovascular Division, Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts 02115
Department of Medicine, Cornell University Medical College, New York 10021
Institute for Muscle Disease, Inc., New York 10021
Find articles by Gorlin, R. in: JCI | PubMed | Google Scholar
Cardiovascular Division, Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts 02115
Department of Medicine, Cornell University Medical College, New York 10021
Institute for Muscle Disease, Inc., New York 10021
Find articles by Wahren, J. in: JCI | PubMed | Google Scholar
Published July 1, 1969 - More info
Myocardial substrate metabolism was studied in 13 subjects at the time of diagnostic cardiac catheterization by means of palmitic acid-14C infusion with arterial and coronary sinus sampling. Two subjects were considered free of cardiac pathology and all, with one exception, demonstrated lactate extraction across the portion of heart under study. Data for this single lactate-producing subject were treated separately.
The fractional extraction of 14C-labeled free fatty acids (FFA) (44.4±9.5%) was nearly twice that of unlabeled FFA (23.2±7.8%) and raised the possibility of release of FFA into the coronary sinus. FFA uptake, based on either the arterial minus coronary sinus concentration difference or the FFA-14C fractional extraction, was directly proportional to the arterial FFA concentration. Gas-liquid chromatography failed to demonstrate selective handling of any individual FFA by the heart. Fractional oxidation of FFA was 53.5±12.7%, accounting for 53.2±14.4% of the heart's oxygen consumption while nonlipid substrates accounted for an additional 30.0±17.3%. Determinations of both labeled and unlabeled triglycerides suggested utilization of this substrate by the fasting human heart.
Direct measurement of FFA fractional oxidation as well as FFA uptake, exclusive of possible simultaneous FFA release, would appear necessary in studies concerned with human myocardial FFA metabolism.