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Thallium-201 and microspheres were injected into the blood simultaneously during left circumflex (LC) occlusion in open chest dogs. The dogs were sacrificed 6-8 minutes later and regional myocardial (201)TI and microsphere concentrations determined. In dogs with permanent LC occlusion the myocardial (201)TI distribution approximated blood flow distribution as judged by the microsphere concentrations. Release of LC occlusion 45 seconds after (201)TI injection almost obliterated the myocardial (201)TI deficit in the area of the LC without changing the microsphere results, presumably a result of deposition of (201)TI during reactive hyperemia. Either delaying the onset of reflow until 3 minutes of attenuating the magnitude of reactive hyperemia by LC stenosis markedly decreased the change in (201)TI distribution due to reflow. We conclude that for a given degree of reversible regional myocardial ischemia at the time of (201)TI injection, the perfusion deficit observed on the initial scintigram will be influenced by the subsequent duration of ischemia and by the magnitude of postischemic reactive hyperemia.

Effect of duration of regional myocardial ischemia and degree of reactive hyperemia on the magnitude of the initial thallium-201 defect.