Uptake of I 131-tagged sodium iodide, triiodothyronine, and thyroxine by experimental myocardial infarcts in dogs

Abstract

Increased radioactivity has been previously detected over the precordial area of patients with myocardial infarcts after the administration of Nal 131. A series of experiments was carried out in dogs to analyze the mechanism of this phenomenon. Infarcts were produced by coronary artery ligation. Twenty-four hours after the administration of Nal 131, the iodide space of infarcted myocardium was 1.7 times greater than that of normal heart muscle. Under the same conditions the ratios of infarcted to normal tissue were 1.5 and 3.3 for radioactive triiodothyronine and thyroxine spaces, respectively. There was also indication that these two iodoaminoacids were deiodinated by both normal and damaged myocardium. Similar results were obtained when normal pectoral skeletal muscle was compared to the damaged muscle at the site of the thoracotomy incision. An incidental finding of this study is that the iodide “space” is twice that reported for chloride. These results indicate that the increase ill the precordial radioactivity over the infarcted myocardium in vivo is clue only in small part to the direct entry of iodide into the myocardium. Maximal uptake should occur after the iodide has been incorporated into endogenous hormone, i.e., thyroxine, which shows the highest concentration differential between normal and damaged myocardium.