动物造模,动脉粥样硬化模型 z-bio 2021-10-12 345

　　(1) Replication method In the 1st and 3rd weeks, 1 ml rabbit Chlamydia pneumonia (Cpn) AR-39 (10IFU/ml) was infected through the nasal cavity to infect male experimental rabbits weighing 2.5 kg. Daily fat diet (with 6% peanut oil, 2% cholesterol, 0.3% bile salt). Before the model, the middle and the end were weighed separately, and the animals' symptoms, diet and two stools were observed every day. Collect 2 ml of blood from fasting ears every two weeks to measure serum CpnIgG antibodies. Blood test first. At the end of the experiment, detect total cholesterol, triacylglycerol, high-density lipoprotein, and low-density lipoprotein; observe the ratio of the As area to the inner membrane area; measure the thickness of the inner membrane; detect rabbit tissue by CpnDNA PCR method. At the end of experiment 12, various degrees of gray-white plaques were found in the aortic intima, distributed in dots, spots, and stripes, with sharp edges. In severe cases, they fuse into thin slices. The collapse of the artery and the inside of the bifurcated blood vessel were observed under an optical microscope. The membrane is obviously thick, and there are many smooth muscle cells proliferating in the inner membrane, and lipid deposits form bubble cells.

　　(2) Model characteristics The results of this model show that rabbits are sensitive to high-fat diet and Cpn. Rabbits infected only with Cpn have no As lesions. More lesions are caused by high fat and Cpn infection. Cpn is more serious than a simple high-fat diet. It can promote and aggravate atherosclerosis in a high-fat diet, and high fat can cause Cpn to infiltrate or colonize the injured intima, indicating that it can promote. Cpn is directly isolated from atherosclerotic plaques in human coronary and carotid arteries. Rabbits and Swisswebster mice are most suitable for studying Cpn infection.

　　(3) Comparative medicine In recent years, the role of Cpn in atherosclerosis has attracted more and more attention, and supports the epidemiology, pathology, molecular biology and related models of Cpn and As in animals. Yes. The test results on this model animal showed that the degree of gray-white plaques on the arterial intima was different, indicating that the intima was significantly thickened. There are lipid deposits in which many smooth muscle cells proliferate in the inner membrane and form foam cells. Vascular disease is consistent with humans. As a symptom, after Cpn infection, T and B lymphocytes may activate autoimmune cardiac inflammatory diseases, and all lung tissues of model animals are interstitial pneumonia. Cpn will exacerbate As.