Objective To detect the opening of the myocardial mitochondrial permeability transition pores (MPTP) after intrauterine asphyxia in neonatal rats,and to explore the mechanism of the myocardial hypoxic-ischemic and reperfusion injury caused by the opening of MPTP after asphyxia.Methods Cesarean sections were undertaken in female SD rats at the 21st day after pregnancy.The uterine arteries were clamped for 30 minutes followed by releasing for 1 hour and the pups were allocated into the asphyxia group.The uterine arteries were isolated but not clamped and the pups were allocated into the control group.There were 30 neonatal rats in either group and all of them were sacrificed 24 h after birth.Serum cardiac troponin Ⅰ (cTn Ⅰ) levels were detected by enzyme linked immunosorbent assay.The opening degree of MPTP was detected by fluorospectro-photometry.Myocardial ischemic areas were detected by TTC staining.Tissues from the cardiac apex were taken and the pathologic changes of the myocardium were explored by hematoxylin-eosin staining.SPSS for Windows 13.0 was used for statistic analyses.Results In HE staining slices,the myocardial cells in asphyxia group were disarranged and edematous.In control and asphyxia group,the serum cTn Ⅰ levels were (0.08 ±0.04) μg/L and (0.40 ±0.29) μg/L (P ＜0.01),the myocardial ischemic areas were (8.01 ±3.48) ％ and (42.50 ± 15.90)％ (P ＜0.01),and the opening degrees of MPTP were (118.10 ± 19.10) RFU and (79.40 ± 10.57) RFU (P ＜ 0.01) respectively.The serum levels of cTn Ⅰ,the myocardial ischemic areas,and the opening degrees of MPTP were significantly increased in asphyxia group compared with control group.The serum level of cTn Ⅰ was positive correlated with the opening degree of MPTP in either group(r =-0.384,P ＜ 0.01).Conclusion There are myocardial injuries in neonatal rats after asphyxia,which represent as high level of serum cTn Ⅰ,myocardial ischemia and necrosis.Opening of the myocardial MPTP is one of the causes of myocardial injury.