Objective：To observe the evolution of pulmonary artery diameters and cardiac functional changes in a rat model of pulmonary artery hypertension（PAH）using 7.0T cardiac magnetic resonance（CMR）. Methods：A rat model of PAH was established by hypoxia. A total of 36 rats were divided into 6 groups on average（baseline，hypoxia at 1st，2nd，3rd，4th，and 5th weeks；n=6）. CMR was performed every week by Bruker BioSpec 7.0T. The diameters of the main pulmonary artery（MPA），right pulmonary artery（RPA），left pulmonary artery（LPA），right ventricular end-diastolic maximum diameter（dRVmax），left ventricular end-diastolic maximum diameter（dLVmax），right ventricular end-diastolic volume（RVEDV）and right ventricular end-systolic volume（RVESV）were measured on MR images；ratio of dRVmax to dLVmax（dRVmax/dLVmax），ratio of the main pulmonary artery to the ascending aorta（MPA/AA，RPA/AA，and LPA/AA），right ventricular and left ventricular ejection fraction（RVEF）were calculated. Right ventricular systolic pressure（RVSP）was obtained by right heart catheterization after CMR imaging for each rat. Comparison of above-mentioned parameters at different time points was calculated by t test and ANOVA analysis（SPSS 24.0）. Pearson correlation analysis was used to evaluate the correlation between above-mentioned parameters and RVSP. Results：The RVSP in model rats at the first week increased significantly compared with the baseline［（29.92 ± 1.94）mmHg vs.（41.55 ± 3.14）mmHg，P＜0.01］，and then gradually increased from the first week to the fifth（P < 0.01）. MPA，dRVmax/dLVmax，RVESV，and RVEDV gradually increased（P＜0.01）. RVEF decreased significantly in the 2nd week of modeling（P < 0.01）. There were moderate correlations between the MPA/AA，dRVmax/dLVmax，RVEF and RVSP in model rats（r=0.573，r=0.700，r=-0.760，all P < 0.01）. Conclusion：7.0T CMR can sensitively observed changes in pulmonary artery diameter and right ventricular function during the progression of PAH rats，which lays a foundation for studying the evolutionary mechanism of PAH.