Background and Objectives: Reperfusion of ischemic myocardium is necessary to salvage tissue from eventual
death. However, new pathophysiological changes are initiated after reperfusion. The aim of this study was to investigate
one of the mechanisms of ischemia/reperfusion (I/R) injury, and we focused on transferrin. Materials
and Methods: Male Spragre-Dawley (SD) rats were used for the I/R model. Myocardial ischemia was produced by
occlusion of the left anterior descending coronary artery for 30 minutes. 99mTc Transferrin-Chitosan-hydrazino
nicotinate hydrochloride (HYNIC) (Tfc) (≒37 MBq/mL) was injected once after the reperfusion was finished.
Autoradiography, hematoxylin and eosin (H & E) staining and determination of the tissue myeloperoxidase (MPO)
activity were performed. Results: Autoradiography showed remarkable 99mTc-Tfc uptake in the left ventricular myocardium
at the reperfusion period from 0 to 1.5 hours, whereas no uptake was demonstrated at 3 hours. The uptake
was increased again at 6 and 24 hours. Western blotting showed that the transferrin receptor (TfR) proteins were
increased at 0 to 1.5 hours compared with that of the control; this expression of TfR disappeared at 3 hours, and
it showed up for the second time at 6 and 24 hours. The MPO activity only at 24 hours was significantly higher than
that of the control and those MPO activities at 0 to 6 hours (p=0.001). Conclusion: In the rodent model of 30
minutes occlusion and reperfusion, our study revealed, with using 99mTc-Tfc, that the TfR expression increased in
the myocardium till 3 hours after reperfusion. TfR-mediated entry of iron into the cardiomyocytes may represent that
this process plays a role in the I/R injury during the early reperfusion period.