Objective：To investigate the release of pro-inflammatory mediators：tumor necrosis factor-α（TNF-α） and intracellular ad－hesion molecules-1（ICAM-1） during myocardial ischemia/reperfusion and related regulatory mechanism. Methods：Totally 30 New Zealand white rabbits were divided into 3 groups：sham group，cardiac ischemia/reperfusion group（the left circumflex coronary arteries of the rabbits were ligated for 90 min then untied for 60 min） and PDTC group（20 mg/kg pyrrolidine dithiocarbamate was injected intravenously 30 min before cardiac ischemia）. Plasma levels of ICAM-1 and TNF-α at different time points during ischemia/reperfusion were detected by ELISA. Myocardial myeloperoxidase activities in different regions were determined and myocardial cell injury was observed under the light microscope and electron microscope. Results：Serum concentration of TNF-α and ICAM-1 in cardiac ischemia/reperfusion group reached the peak 150 min after myocardial ischemia，which was significantly higher than that of sham group and PDTC group（P<0.05）. Myeloper－oxidase in no-reflow area and ischemic area was significantly higher in ischemia/reperfusion group than in sham group and PDTC group（P<0.05）. Histological results showed that myocardial injury in no-reflow area was less severe in PDTC group than in ischemic/reperfusion group. Conclusions：Cardiac ischemic/reperfusion can promote the release of pro-inflammatory mediators. Inhibition of nu－clear factor-κB can decrease the infiltration and activation of neutrophile granulocyte，attenuate the release of pro-inflammatory factors and decrease myocardial injury in no-reflow area.