Postoperative intimal hyperplasia is still the major cause of vein graft occlusion. No medicine, however, can suppress the development of postoperative intimal hyperplasia. Since June 2001, edaravone has been commercially available as the free radical scavenger for acute cerebral infarction. In addition, it is well known that edaravone in lower dosage also suppresses injury to endothelial cells of vessels in vitro. In this study we evaluated the effect of edaravone on the development of postoperative intimal hyperplasia in a rat model. In ten male rats (498 ± 53 g) we interposed the right epigastric vein graft into the common femoral artery. The ten rats were divided into two groups: edaravone group (n = 5) in which there was the preoperaiive administration of edaravone (3.0 mg/kg) into peritoneal cavity, and the control (n = 5) in which the same dose of saline was used. After 4 weeks three sections were taken from the vein grafts and stained with Verhoeff's and van Gieson's stains. The intimal areas of the vein graft were measured using computerized planimetry. The averages of the intimal area and serum monocyte chemoattractant protein 1 (MCP-1) level were compared between the two groups. The mean ischemic time was 68 ± 6 min. The average of the intimal area in the edaravone group was significantly lower than the control group (0.05 ± 0.02 mm2 vs. 0.43 ± 0.05 mm2, p &lt
0.001). The average of serum MCP-1 in the edaravone group was also significantly lower than that of the control group (116 ± 11 pg/mL. vs. 169 ± 10 pg/mL, p &lt
0.01). Our results suggested that edaravone could suppress postoperative intimal hyperplasia of the vein graft in a rat model.