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Mechanism of Localization of ^99mTc-Labeled Pyrophosphate and Tetracycline in Infarcted Myocardium

Tufts University School of Medicine and New England Medical Center, Boston, Massachusetts

Correspondence: For reprints contact: Mrinal K. Dewanjee, Dept. of Radiology, Div. of Nuclear Medicine, 171 Harrison Ave., New England Medical Center, Boston, MA 02111.

ABSTRACT

The gross and subcellular localizations of ^99mTc-labeled pyrophosphate and tetracycline in myocardial infarcts were studied in a rabbit model. Experiments utilizing double-nuclide labeling were carried out using a useful mapping technique. Concentration of the various chelates decreases in an expected manner from the center of the infarcted area toward its periphery, but it is higher near the epicardial surface than toward the endocardium. Technetium-99m-pyrophosphate is concentrated in the same infarcted areas as ⁴⁵Ca ion or ³²P-pyrophosphate, but to a much greater degree. The uptake is dependent on both the degree of necrosis and residual blood flow. Gel filtration experiments with rabbit serum indicate that ^99mTc-tagged pyrophosphate, tetracycline, and diphosphonate are mainly protein-bound, whereas ³²P-pyrophosphate is not. Subcellular localization studies show that ^99mTc-tetracycline and ^99mTc-pyrophosphate are bound primarily to soluble protein, and only a small fraction is associated with nuclei, mitochondria, and microsomes. The uptake of technetium chelates in myocardial infarcts may be due to the formation of polynuclear complexes with denatured macromolecules rather than to the deposition of calcium in mitochondria.

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