MECHANISM OF LOCALIZATION OF TC-99M-LABELED PYROPHOSPHATE AND TETRACYCLINE IN INFARCTED MYOCARDIUM

  • 1 January 1976
    • journal article
    • research article
    • Vol. 17  (7) , 639-646
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 decreased in an expected manner from the center of the infarcted area toward its periphery, but it was higher near the epicardial surface than toward the endocardium. Technetium-99m-pyrophosphate was concentrated in the same infarcted areas as 45Ca2+ or 32P-pyrophosphate, but to a much greater degree. The uptake was dependent on both the degree of necrosis and residual blood flow. Gel filtration experiments with rabbit serum indicated that 99mTc-tagged pyrophosphate, tetracycline and diphosphonate were mainly protein-bound; 32P-pyrophosphate was not. Subcellular localization studies show that 99mTc-tetracycline and 99mTc-pyrophosphate were bound primarily to soluble protein, and only a small fraction was 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 Ca in mitochondria.

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