Despite extensive clinical use of thallium-201 (201TI) for myocardial imaging, the effect of ischemia on myocardial accumulation and release of 201TI independent of flow has not been fully defined. Therefore, myocardial accumulation of 201TI in response to ischemic-like myocardial injury was assessed in vitro using the cultured fetal mouse heart preparation. Cultured fetal mouse hearts (n = 311) were subjected to injury simulating ischemia by deprivation of oxygen and oxidizable substrates for periods ranging from 15 minutes to 10 hours. The extent of irreversible injury was determined by the percentage of lactic dehydrogenase (LDH) lost from the hearts to the culture medium during recovery from injury. Injury was essentially reversible at 1 hour of insult. The fraction of 201TI content in injured compared with control hearts was not significantly lower after 1 hour of insult. By 3 hours of insult, irreversible injury as assessed by loss of LDH was detectable and the extent of injury increased progressively through 10 hours. During the 3-10-hour period of irreversible injury, 201TI accumulation within injured hearts compared with controls was related in a monotonically decreasing fashion to the loss of LDH as described by a mathematical kinetic model that fit the observations closely (R2 greater than 0.99). These results indicate that in this organ culture preparation, in which there is effectively an unlimited reservoir of 201TI and no confounding effects of perfusion, the time-dependent 201TI accumulation is determined by the extent of irreversible injury.
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