ObjectiveTo explore the effects of sophoridine on cardiac function and myocardial ultrastructure of rats with myocardial infarction. MethodsThe SD rat model of myocardial infarction (MI) was obtained by permanent ligation of the left anterior descending coronary artery (LAD), and the model rats were randomly divided into model group (rats with MI), low-dose group (5 mg/kg sophoridine), middle-dose group (10 mg/kg sophoridine), and high-dose group (20 mg/kg sophoridine); a sham operated group was also included. Each group had 10 rats. The elevated left ventricular end-diastolic pressure (LVEDP), ±dp/dtmax and heart mass/body mass (HM/BM) were determined after experiment, and the changes of myocardial ultrastructure were observed by transmission electron microscope. ResultsCompared with the sham operated group, ±dp/dtmax in MI group was significantly decreased, and LVEDP and HM/BM were remarkably increased (all P<0.01). Compared with MI group, ±dp/dtmax in the 3 sophoridine groups were significantly increased, and LVEDP and HM/BM were significantly decreased (P<0.01, P<0.05), except for -dp/dtmax in the low-dose sophoridine group. Transmission electron microscope found that the myofilaments of myocardial cells in the sham operated group were well arranged, with normal mitochondria. The myofilaments were dissolved in MI rats, with swollen mitochondria and blurred cristae, showing distinct pathological changes. There was a slight improvement in myofilament dissolution in the low-dose sophoridine group, and the myofilament dissolution disappeared in the middle- and high-dose group, with well arranged myofilaments. ConclusionSophoridine can improve the cardiac function of MI rats, and has protective effects on ultrastructure of myocardial cells.