Abstract: BACKGROUND: Myocardial infarction is the most serious clinical type of coronary heart disease. The development of anti-myocardial ischemia drugs has become a research hotspot. Establishing an appropriate animal model and investigating its pathophysiological mechanism can provide an effective tool for pharmacodynamics evaluation in new drug development and promote the development of anti-myocardial infarction drugs for myocardial infarction. 
OBJECTIVE: To evaluate the changes of cardiac function, tissue morphology and cardiomyocyte ultrastructure in rats after acute myocardial infarction. 
METHODS: Thirty male Sprague-Dawley rats were randomly divided into two groups (n=15 per group): a sham surgery group and a model group. Rats in the model group were subjected to ligation of the left anterior descending coronary artery, while in the sham surgery group, the left anterior descending coronary artery was only threaded without ligation. On the 7th, 14th, and 28th days after modeling, changes of ST segment in lead II were observed by electrocardiogram, and the general changes of the heart were observed by thoracotomy. Myocardial infarction area was determined by 2,3,5-triphenyltetrazolium chloride staining. Hematoxylin-eosin staining was used for pathological observation of the heart, and Masson staining was adopted for the determination of myocardial fibrosis degree. Moreover, the cardiomyocyte ultrastructure was observed by transmission electron microscope. 
RESULTS AND CONCLUSION: Compared with the sham surgery group, the results of electrocardiogram showed that the J point was obviously elevated on the 7th day, and the Q wave waveform was broadened and the amplitude was increased on the 14th day. The gross observation of the heart showed that rats in the model group had left ventricular hypertrophy on the 7th and 14th days and cardiac atrophy on the 28th day after operation. The results of 2,3,5-triphenyltetrazolium chloride staining showed myocardial infarction area in the model group was increased progressively. Hematoxylin-eosin and Masson staining results indicated that myocardial cells arranged disorderly, accompanied by myocyte necrosis, inflammatory cell infiltration, and fibrous proliferation that were gradually aggravated. Under the transmission electron microscope, the mitochondrial swelling was worsened in the cardiomyocytes, and the number of mitochondrial cristae was significantly reduced. All these findings reveal that the changes of cardiac function, tissue morphology, and ultrastructure of cardiomyocytes in the Sprague-Dawley rat model of myocardial infarction accord with the occurrence and development of myocardial infarction, which can provide experimental evidence for the development of therapeutic drugs for myocardial infarction.

Key words: myocardial infarction, coronary artery, left anterior descending artery, electrocardiogram, animal model, rat