Résumé
Acute myocardial infarction is one of the major causes of death in the world. Research on animal models of myocardial infarction has a great significance in improving the pathophysiology, diagnosis and treatment of human myocardial infarction. At present, problems such as low survival rate and complicated preparation still exist. In recent years, some progress has been made in the preparation of animal myocardial infarction models, which can improve the survival rate, qualified rate and speed. This paper analyzes the preparation of rat models of acute myocardial infarction and related research, combined with actual factors to simplify the process of preparation and improve the skills of scientific researchers, so as to provide a source of stable and reliable acute myocardial infarction models for medical research.
Résumé
Acute myocardial infarction is one of the major causes of death in the world. Research on animal models of myocardial infarction has a great significance in improving the pathophysiology, diagnosis and treatment of human myocardial infarction. At present, problems such as low survival rate and complicated preparation still exist. In recent years, some progress has been made in the preparation of animal myocardial infarction models, which can improve the survival rate, qualified rate and speed. This paper analyzes the preparation of rat models of acute myocardial infarction and related research, combined with actual factors to simplify the process of preparation and improve the skills of scientific researchers, so as to provide a source of stable and reliable acute myocardial infarction models for medical research.
Résumé
Objective To establish a Juema minipig model of myocardial infarction, to evaluate the clinical indi?ces in the model pigs, and to explore the relationship between gene expression and metabolic decompensation. Methods 13 male Juema minipigs were randomly divided into control (Sham, n=5), myocardial infarction (MI, n=5) and normal control (for evaluating the recovery condition after surgery, n=3) groups. In the MI group, the ligation was done at the left descending coronary artery around the 1/3 distance to heart apex. Four weeks after the surgery, the cardiac function and serum biochemistry was analyzed. The histological changes and gene expression profiles in the myocardium in the peri?infarct area were exanimated. Results Ultrasonic images showed that the infarction was formed, the ejection fraction and fraction shortening were significantly reduced in the MI group ( ~32% and ~40% less than those of the sham group). Histological examination showed that myocardial fibers at the peri?infarct area were broken, dissolved, and there was con?nective tissue hyperplasia with increased neutrophil and lymphocyte infiltration. Microarray analysis revealed that two myo?cardial remodeling and pathology mediating pathways, three inflammation?related pathways, and 8 metabolic pathways ( in?cluding fatty acid, amino acid, and glucose metabolic pathways) were significantly changed. Conclusions We have suc?cessfully established a Juema minipig model of myocardial infarction. The less branches of the left descending coronary ar?tery allow us to establish a stable model by surgery with comparable characteristics in the clinic indices. The results of this study provides useful reference characteristics of an animal model with characteristic changes in the peri?infarct area.
Résumé
Objective: To study the effect of berberine (BR) on ventricular remodeling in experimental rats with myocardial infarction (MI) and its mechanisms. Methods: The MI model of experimental rats was established by ligation of the left anterior descending coronary artery and the MI animals were randomly divided into 3 groups: MI+BR group, in which the rats received BR 20 mg/kg.d, Sham group and MI group, the rats in those 2 groups received the same volume of normal saline. All animals were treated for 8 weeks. The cardiac function and structure were assessed by echocardiography, cardiac interstitial collagen deposition was evaluated by Masson stain, the myocardial cell apoptosis was detected by Tunel method, and the activation of nuclear factor (NF-κB) was also examined. Results: For echocardiography, MI group had enlarged left ventricular end diastolic diameter (7.28 ± 0.29) mm than Sham group (6.86 ± 0.36) mm,P0.05. MI group had increased left ventricular end systolic diameter (5.88 ± 0.33) mm than Sham group (4.61 ± 0.31) mm, but it decreased in MI+BR group (4.68 ± 1.17) mm, allP Conclusion: Application of BR may improve the ventricular remodeling and cardiac function in experimental MI rats, it might be because of BR partially inhibit NF-κB activation, reduce collagen deposition and help anti-apoptosis in myocardial cells.
Résumé
Objectives: The purpose of study is to evaluate serial MR imaging of myocardial infarction using non-surgical model of myocardial infarction after percutaneous transcatheter coronary arterial embolization in dogs. MATERIALS AND METHODS: We evaluated serial pre- and post-contrast MR images with Gd-DTPA (gadolinium-diethylenetriamine-pentaacetic acid) of heart of the eleven mongrel dogs (immediate group (n=3), one week group (n=3), three weeks group (n=5)) after making non-surgically induced myocardial infarction. We confirmed the infarct with TTC staining and microscopically. The location and extents of the myocardial infarction were correlated. RESULTS: A total of 24 MR images were archived; 11 images of the immediate post-embolic period, 8 images of one-week follow-up, and five of 3-week follow-up images. Comparing with the signal intensity of normal myocardium, immediate post-embolic MR images showed low or iso signal intensities (SI) of the infarct area on T1-weighted images (T1WI) and high SI on T2-weighted images (T2WI). No contrast enhancement with Gd-DTPA was made in all cases of the immediate post-embolic MRI. One-week and 3-week follow-up MR images showed low or iso SI on T1WI and slight high or iso SI on T2WI. Contrast enhancement images in both one-week and 3-week follow-up MRI showed denser enhancement of infarct area in one-week follow-up. The myocardial wall thinning was seen in 5 of eight dogs after one week and in 3 of five after 3 weeks. CONCLUSION: In non-surgical animal models of myocardial infarction, MR images showed low or iso SI on T1WI, and high SI on T2WI in various stages, and contrast enhancement was maximum after one week and gradual decrease to 3 weeks. The myocardial wall thinning was seen in one-to 3-week follow-up MR images.