Myocardial Extraction of Labeled Long-Chain Fatty Acid Analogs

Poe, Norman D.; Robinson, G. D.; MacDonald, Norman S.

doi:10.3181/00379727-148-38509

Cited by 56 publications

(13 citation statements)

References 4 publications

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“…When labeled at the end of the carbon chain with radioiodine, their pharmacokinetic behaviour closely resembles that of the normal FFAs (15,20,24). The use of the radiophysically ideal isotope 123 I as the label gives access to an interesting class of radiopharmaceuticals.…”

Section: Introductionmentioning

confidence: 83%

“…No difference was observed in uptake between 1 3 1 I-HDA and 1 3 1 I-PPA, either when injected separately or as a mixture. The high uptake of 1 3 1 I-HDA, which is comparable to the uptake of normal naturally occurring FFA, could be explained by the similarity of the terminal iodine to a methyl group (15,20,24). Therefore it seems that the presence of the bulky 4iodophenyl group at the end of the carbon chain does not make any difference either.…”

Section: Myocardial Uptakementioning

confidence: 97%

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Myocardial Uptake of Iodinated Free Fatty Acids and 201T1 in Experimental Ischemia

Westera¹,

Visser²,

Scholtalbers³

et al. 1984

Nuklearmedizin

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SummaryIn an experimental study, we evaluated the uptake of (131I)-17-iodo heptadecanoic acid (131I-HDA), (125I)-15-4 (4-iodophenyl) pentadecanoic acid (125I-PPA) and thallium-201 (201T1) in the dog heart. Twenty dogs were studied and divided into 3 groups: in group A, 10 dogs (4 normal, 6 with coronary artery occlusion) were studied with 131I-HDA and 201T1; in group B, 5 dogs (with occlusion) received 125I-PPA and 201T1; and in group C, 5 dogs (with occlusion) were studied with 125I-PPA and 131I-HDA. Two min after administration of the compounds the hearts were excised and stored in formaldehyde. After sectioning of the left ventricle, total uptake was counted and expressed in percentage of injected dose. Uptake in the normal myocardium (group A) was 4.2 ±0.6% for 131I-HDA and 4.6 ±0.7% for 201T1; in the occluded dog hearts (group A) we measured values of 2.6 ±0.4% for 131I-HDA (p<0.001) and 3.4 ±0.6% for 201T1 (p<0.01). Uptake of 131I-HDA, 125IPPA and 201T1 in groups B and C was not significantly different: group B, 125I-PPA 2.8 ±0.8% and 201T1 ± 0.5%; group C, 125I-PPA 1.9 ±0.7% and 131I-HDA 1.6 ±0.6%. Moreover, regional distribution of both iodinated fatty acids was quite comparable with the distribution of 201T1. We conclude that 131I-HDA and 125I-PPA show similar uptake as 201T1 and are distributed according to coronary artery perfusion, which underscores their value as myocardial imaging agents.

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Section: Introductionmentioning

confidence: 83%

Section: Myocardial Uptakementioning

confidence: 97%

Myocardial Uptake of Iodinated Free Fatty Acids and 201T1 in Experimental Ischemia

Westera¹,

Visser²,

Scholtalbers³

et al. 1984

Nuklearmedizin

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“…It has previously been shown that especially non-selective beta-blockers reduce plasma FFA levels by counteracting the beta-adrenoceptor mediated lipolysis (18,5,6,27,35) and also reduce myocardial FFA uptake (9,14,22). Accordingly, the purpose of this study was to evaluate the influence of different beta-blockers on the myocardial FFA uptake in the normal and occluded dog heart by using radioaetively labeled iodoheptadecanoic acid ( 1 3 1 I-HDA), a stearic acid analogue with similar metabolic behaviour as the normal compound (26,13). This radioactive procedure enabled us to study both total FFA uptake and regional FFA distribution (36).…”

Section: Zusammenfassungmentioning

confidence: 99%

Metabolic Consequences of Beta-Adrenergic Receptor Blockade for the Acutely Ischemic Dog Myocardium

Westera¹,

Wall²,

Eenige³

et al. 1984

Nuklearmedizin

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SummaryIn an experimental study in 50 dogs the myocardial uptake of free fatty acids (FFAs) after beta-blockade was determined using radioiodinated heptadecanoic acid as a metabolic tracer. All 4 beta-blockers used (metoprolol, timolol, propranolol and pindolol) lowered the uptake of FFAs in the normal canine heart. Uptake of FFAs was also diminished after coronary artery occlusion per se, but administration of beta-blockers exerted little additional influence on the uptake of FFAs. This observation was qualitatively parallelled by the uptake of 201T1 in concomitant experiments. Plasma FFA levels were increased by pindolol (non-selective with intrinsic sympathomimetic activity), not changed by metoprolol (a cardioselective betablocking agent) and lowered by timolol and propranolol (both nonselective compounds). The extent of ischemic tissue, as reflected by uptake of iodoheptadecanoic acid and 201T1, was diminished by metoprolol but not by other beta-blockers. Regional distribution of both tracers, as shown in the endo-epicardial uptake ratios, was hardly influenced by beta-blockade, except for a small increase of 201T1 uptake in non-occluded endocardium. Uptake of 201T1 as well as of iodoheptadecanoic acid in the ischemic area was increased by metoprolol, timolol and propranolol and decreased by pindolol. We conclude that beta-blocking agents confer different effects on myocardial uptake and metabolism of FFAs which might possibly be related to their different inherent properties.

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“…The first fatty acid labelled with iodine-131 for myocardial imaging was oleic acid [1]. Thereafter, several fatty acids were labelled with halogen [2,3]. In the search for a technique for analysing myocardial lipid metabolism, pharmacokinetic studies in mice revealed that co-halo fatty acids, especially 17-I-heptadecanoic acid (IHA), were taken up and eliminated from the myocardium in a manner similar to palmitic acid (PA) [3].…”

Section: Introductionmentioning

confidence: 99%

Beta-oxidation of 1-[14C]-17-[131I]-iodoheptadecanoic acid following intracoronary injection in humans results in similar release of both tracers

et al. 1993

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Radioiodine labelled 17-iodo-heptadecanoic acid (IHA) is used for non-invasive study of myocardial metabolism in coronary heart disease and cardiomyopathy. Yet in the interpretation of in vivo myocardial tracer kinetics, it is controversial whether the intracellular degradation of IHA or the removal of iodide across cellular membranes is the rate-limiting step in iodide release from the myocardium. In five patients undergoing coronary sinus catheterization, a mixture of about 40 kBq of [123I] NaI was injected into the left coronary artery. During the following 15-min period, frequent blood samples were taken from the aorta and the coronary sinus. In the aqueous phase of the venous blood, 14CO2 and inorganic 131I appeared nearly in parallel, with a peak time of 4-5 min. Moreover, as shown by the AV difference, there was no significant back diffusion of IHA and no significant non-specific deiodination detectable over the period of observation. There was myocardial retention of inorganic iodide (123I) injected into the left coronary artery. The data strongly support the premise that lipid turnover through beta-oxidation is the rate-limiting step in the externally measured release of iodide after IHA injection, provided that recirculating inorganic radioactive iodide is corrected for. In addition, 15 volunteers were studied using [11C]palmitic acid and [123I]IHA using PET and dynamic planar camera scintigraphy with iodide correction. There was no significant difference between the mean values of the elimination half-times, and also no significant correlation between half-times of both fatty acids for single individuals.

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Myocardial Extraction of Labeled Long-Chain Fatty Acid Analogs

Cited by 56 publications

References 4 publications

Myocardial Uptake of Iodinated Free Fatty Acids and 201T1 in Experimental Ischemia

Myocardial Uptake of Iodinated Free Fatty Acids and 201T1 in Experimental Ischemia

Metabolic Consequences of Beta-Adrenergic Receptor Blockade for the Acutely Ischemic Dog Myocardium

Beta-oxidation of 1-[14C]-17-[131I]-iodoheptadecanoic acid following intracoronary injection in humans results in similar release of both tracers

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