The Fate of 131I-17-lodohepta-decanoic Acid During Lactate Loading: Its Oxidation is Strongly Inhibited in Favor of its Esterification

C. M. B. Duwel; F. C. Visser; M. J. van Eenige; W. Den Hollander; J. P. Roos

doi:10.1055/s-0038-1629508

Nuklearmedizin - NuclearMedicine, Table of Contents

Nuklearmedizin 1990; 29(01): 24-27
DOI: 10.1055/s-0038-1629508

Originaler Artikel

Schattauer GmbH

The Fate of ¹³¹I-17-lodohepta-decanoic Acid During Lactate Loading: Its Oxidation is Strongly Inhibited in Favor of its Esterification

A Radiochemical Study in the Canine Heart

C. M. B. Duwel

¹ The Department of Nuclear Medicine, Free University Hospital, Amsterdam, The Netherlands

,

F. C. Visser

¹ The Department of Nuclear Medicine, Free University Hospital, Amsterdam, The Netherlands

,

M. J. van Eenige

¹ The Department of Nuclear Medicine, Free University Hospital, Amsterdam, The Netherlands

,

W. Den Hollander

^*From the Department of Cardiology, Free University Hospital, Amsterdam, The Netherlands

,

J. P. Roos

¹ The Department of Nuclear Medicine, Free University Hospital, Amsterdam, The Netherlands

› Author Affiliations

Abstract

The influence of lactate loading on fatty acid metabolism (pH = 7.4) by the normal canine heart was investigated radiochemically using the radioiodinated fatty acid ¹³¹I-17-iodoheptadecanoic acid (¹³¹I-17-HDA). Fatty acid metabolism was studied during control conditions (n = 8) and after lactate loading (n = 7). In the canine heart total myocardial¹³¹I-17-HDA radioactivity (uptake) was not changed during the lactate intervention. The oxidation decreased fivefold (measured as free ¹³¹I-iodide ion) from 70% to 14% (p < 0.0001, Student’s t- test). Thin-layer chromatography of cardiac lipids demonstrated that the nonoxidized ¹³¹I-17-HDA was mainly stored in the triglycerides and phosphoglycerides. These results suggest that lactate inhibits cardiac ¹³¹I-HDA oxidation.

Zusammenfassung

Der Einbau von ¹³¹J-17-Jod-Hepta- dekansäure (¹³¹J-17-HDA) wurde am gesunden Hundeherz unter Kontroll- bedingungen (n = 8) und nach Zugabe von Laktat (n = 7) untersucht. Der Gesamtwert der myokardialen ¹³¹J-17- HDA-Aufnahme war unter Laktatinfusion unverändert. Die Oxidation verringerte sich um das Fünffache (gemessen am freien ¹³¹J-Jodid), nämlich von 70 auf 14% (p <0,0001). Die Dünnschicht-Chromatographie der myokardialen Lipide zeigte, daß nicht- oxidierte ¹³¹J-17-HDA hauptsächlich in Triglyzerid und die Phosphorglyzeride eingebaut wurde. Diese Ergebnisse weisen auf eine Laktat-vermittelte Inhibition der Oxidation von ¹³¹J-17- HDA hin.

Full Text

References

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