| Pathological cardiac hypertrophy is one of adaptive responses of the heart to a variety of pathological stimuli, and always one of the complications of some cardiovascular diseases, such as hypertension, myocardial infarction, congenital heart diseases, cardiovalvular diseases, and etc. It is well accepted that the formation of cardiac hypertrophy is bound up with extracellular stimuli, intracellular signal transduction and subsequent activation of DNA's transcription. Recently, researchers gradually have deeper insight into alterations of heart functions and genic expression when cardiac hypertrophy happens, but the detailed mechanism relative to formation of cardiac hypertrophy remains unclear. Mophological studies have demonstrated that, pathological cardiac hypertrophy is characterized not only by hypertrophy of cardiomyocytes, but also by proliferation of interstitial cells and accumulation of collagen. Accordingly, studies on signal transduction molecules relative to cellular effects mentioned above are necessary for better understanding of cardiac hypertrophy. In view of the diversity of animal models with cardiac hypertrophy and different stabilities of different models, some of conclusions relative to cardiac hypertrophy don't correspond with each other. Thus, this study is firstly aimed to discuss the fabrication and evaluation of rat models with cardiac hypertrophy, and then the expression's alterations of certain signal transduction molecules relative to formation of cardiac hypertrophy and its regression under the influence of L-arginine in rat models with abdominal aortic stenosis are respectively observed, in order to clarify the relationship between cardiac hypertrophy and signal transduction molecules, and interpret the mechanism of L-arginine's effects on pathological cardiac hypertrophy.1 Study of fabrication and evaluation of rat models with cardiac hypertrophy induced by abdominal aortic stenosisObjectives: This experiment is designed not only to evaluate two different operation modes used in making rat models with cardiac hypertrophy, but also to clarify different influences of different degrees of abdominal aortic stenosis on survival rate and the level of cardiac hypertrophy and hypertension. Our study is aimed to improve the model-making method which is widely applied in the research field of pathological cardiac hypertrophy. Methods: 1. The survival rate of one group with traditional operation mode is compared with that of another group with revised operation mode. 2. After comparison, the operation mode with higher survival rate is selected, and then is utilized to operate on abdominal aortas of other four rat groups. The abdominal aortas' internal diameters of these four groups are respectively coarctated to 0.5mm, 0.6mm, 0.7mm and 0.8mm according to different groups (These four groups are briefly called 0.5mm group, 0.6mm group, 0.7mm group and 0.8mm group respectively in accordance with the internal diameter of abdominal aorta after coarctation). Four weeks after the operation, the survival rates of these four groups are compared with each other. 3. Using some indexes such as left ventricular mass index (LVMI), the left ventricular wall thickness (LVWT), the diameter of cardiac myocyte (DCM) and mean arterial blood pressure (MABP), we compare the level of cardiac hypertrophy and hypertension in 0.8mm group with that in 0.7mm group and sham group four weeks after the operation. Results: 1. Four weeks after the operation, the survival rate in the group with revised operation mode was higher than that in the group with traditional operation mode. 2. Four weeks after the revised operation mode was adopted for 0.5mm group, 0.6mm group, 0.7mm group and 0.8mm group, the survival rate in 0.8mm group was higher than that in any other three groups. 3. Four weeks after the revised operation mode was adopted, compared with the rats in sham group, the rats in 0.7mm group and 0.8mm group have formed obvious cardiac hypertrophy and hypertension. As for the level of cardi... |
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