Scintigraphic imaging of programmed cell death, apoplcssis, in ischemic myocardium

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To determine the time course, location and extent of this process in various severity of ischemia we studied ^<99m>Tc-annexin-V uptake in groups of rats following various intervals of coronary occlusion (20, 15, 10, 5 min) and reperfusion time (0.5, 1.5, 6, 24 hr, 3 day, 14 day). After reperfusion ^<99m>Tc-annexin-V was injected and 1 h later the rats were sacrificed. Dual tracer autoradiography was performed to assess ^<99m>Tc-annexin-V uptake and area at risk. In all 5-min occlusion and reperfusion models, no significant ^<99m>Tc-annexin V uptake was observed in the area at risk. In 10-min, 15-min, and 20-min ischemia and reperfusion models, significant ^<99m>Tc-annexin V uptake was observed depending on the severity of ischemia and reperfusion time. In each group of rats with the same reperfusion time, ^<99m>Tc-annexin V uptake depended on the severity of ischemia ; higher uptake in longer occlusion time. In each group of rats with the same ischemic time, ^<99m>Tc-annexin V uptake was highest in 0.5 h reperfusion model and the uptake decreased time dependently. In 20-min ischemia, a certain level of histological evidence of infarction was observed. In 15, 10, 5-min ischemia, there was no significant histological change was observed in 10-min and 5-min ischemia group. These data indicate that annexin binding depends on the severity of ischemia which results in the wide spectrum of histological change ; that is from infarction to no significant histological change. ^<99m>Tc-annexin V imaging may be feasible in the assessment of acute myocardial ischemia without infarction as well as infarction.