Fucoidan, a sulfated polysaccharide extracted from brown seaweed, is a candidate for the treatment of ischemic diseases. The aim of this study was to measure the therapeutic potential of fucoidan in a rat model of myocardial ischemia–reperfusion injury. Forty rats were submitted to myocardial ischemia–reperfusion injury by transient occlusion of the left coronary artery. Rats were then randomized into 2 groups: fucoidan (5 mg/kg, intramuscularly; n = 20) or control (saline intramuscularly; n = 20) was administered 1 hour before injury and daily thereafter for 1 month. At 1 month, plasma levels of stromal cell–derived factor-1α (SDF-1α) were assessed by enzyme-linked immunosorbent assay kit. Hearts were evaluated by histoimmunochemistry. Fucoidan induced significant antifibrotic effects, reducing the infarct scar size by almost 30% on Sirius red–stained sections (9.45% ± 4.27% vs. 13% ± 5.67% in controls; P = 0.03). Vascular density in the fucoidan group (α-actin, RECA-1, or lectin BS1 stained) was increased by 40% (2.18 ± 0.79 mm2 vs. 1.49 ± 0.42 mm2 in controls ×200; P = 0.001). Plasma SDF-1α at 1 month was not significantly different between the 2 groups. However, increased immunostaining density of SDF-1α and vascular endothelial growth factor in fibrotic ischemic tissues was observed in fucoidan-treated animals versus controls. In conclusion, fucoidan enhanced tissue repair in myocardial ischemia–reperfusion by promoting revascularization (in situ vascular endothelial growth factor and SDF-1α overexpression) and limiting fibrosis. Consequently, fucoidan may be useful for myocardial ischemic patients.