Hypoxia inducible factor-1α (HIF-1α) plays important roles in the regulation of transcriptional responses to hypoxia. In this study, the expression of HIF-1α gene and its downstream gene vascular endothelial growth factor (VEGF) in ischaemic myocardium and the effects of adenovirus mediated transgenic HIF-1α on cardiac function and myocadiocyte apoptosis after acute myocardial infarction (AMI) were investigated. Rabbits performed experimental AMI were divided into four groups randomly and Ad-HIF-1α, Ad-Blank and Rz-HIF-1α were transfected respectively. Sham group was regarded as control. The ultramicrostructure of ischaemic myocardium was observed by electron microscope and light microscope. The mRNA expression of HIF-1α and VEGF was detected by RT-PCR at different time point. The protein expression of HIF-1α, VEGF and CD31was detected by the means of immunohistochemistry and western-blot. The cardiac function of rabbits in each time point were detected by Maclab/8s. Cardiomyocyte apoptosis was detected with TUNEL method at different time point. It was found that the mRNA and protein expression of HIF-1α and VEGF increased at 1d post-infarction, with the peak at 7 d and decreased gradually at 14 and 28 d. At 56 d, HIF-1α mRNA and protein were undetectable, but VEGF mRNA and protein still expressed. The cardiac functional parameter was the highest in Sham group, and the lowest in Rz-HIF-1α group. It was higher in Ad-HIF-1α than in Ad-Blank group. The number of apoptotic cells was the most in Rz-HIF-1α group, and it was less in Ad-HIF-1α than in Ad-Blank group. The number of apoptotic cells decreased with extension of time. There was little apoptotic cells in Sham group. From all above, it was concluded that Ad-HIF-1α could be tranfected and activated effectively. Rz-HIF-1α could suppress the expression of HIF-1α and VEGF. The cardiac function could be improved by Ad-HIF-1α and deteriorated by Rz-HIF-1α. Cardiomyocyte apoptosis could be inhibited by Ad-HIF-1α and increased by Rz-HIF-1α.