Reperfusion of ischemic myocardium is necessary to salvage tissue from eventual death. However, new pathophysiological changes were initiated after reperfusion. The aim of this study was to investigate one of the mechanisms of ischemia/reperfusion (IR) injury, focused on the iron transporter, transferrin, at the affected myocardium. Male SD rats, weighing 250 to 300 g, were used for IR model. Myocardial ischemia was produced by occlusion of the left anterior descending coronary artery for 30 minutes. Once the reperfusion finished, 99mTc Transferrin (��� 37 MBq/ml) was injected through the left external jugular vein. After 30 minutes, the hearts were harvested. Autoradiography, immunohistochemical determination of TfR, and tissue myeloperoxidase (MPO) activity were performed. Autoradiographys showed remarkable radioactivity uptake in the left ventricular myocardium at reperfusion duration of 0 to 1.5 h, whereas at 3 h, any uptake did not shown. At 6, and 24 h, the uptake was increased again. The results of western blot showed that TfR proteins were increased at 0 to 1.5 h compared with that of control, disappeared at 3 h, and showed at 6, and 24 h for the second time. MPO activity at only 24 h was significantly higher than control and those at 0 to 6 h (P=0.001). In the rat model of 30-min occlusion, inflammatory cell infiltrates did not mainly participate in myocardial damage till 3 h after reperfusion. TfR-mediated entry of the iron into cardiomyocytes may represent that it play a role in reperfusion damage in the early reperfusion period (< 3 h). A greater understanding of TfR mediated pathophysiologic process in the IR model will provide a key in the development of new therapeutic strategy for coronary artery disease.