动物造模,动脉粥样硬化模型 z-bio 2021-03-22 314

　　(1) Breeding method Male Wistar rats weighing 180-200g were injected intraperitoneally with vitamin D 600,000U/kg body weight once, and fed with a basic diet. On the 34th day after the injection of vitamin D, anesthetize with 300 ml sodium pentobarbital, 1% paraformaldehyde and 1.25% glutaraldehyde solution, and perfuse the left ventricle by intubation, then immediately cut the aorta into paraffin sections, HE Staining and ultrathin section collection and observation. Under the optical microscope and electron microscope. The proliferation of smooth muscle cells in the aortic wall of the animal is obvious, the location of the cells is disordered, the structure of the elastic fiber layer is unclear, and the local tube wall protrudes into the lumen, typically forming atherosclerotic plaques. There are many collagen fibers between the proliferation of collagen fibers and smooth muscle cells under the aortic endothelium, and foam cells can be seen under the endothelium. Another method is to take 3.4 million U/kg body weight of vitamin D orally into the stomach within 0, 24, and 48 hours and feed on a standard diet. After administering 3.4 million U of vitamin D into the stomach for 9 weeks, arterial slices showed medial edema and calcification, medial smooth muscle hyperplasia, intimal injury and subintimal calcification.

　　(2) The characteristics of the model: Compared with the previous models that caused animal vitamin D to cause atherosclerosis, this model has the advantages of easier operation, lower cost, shorter time, and higher success rate. This model has a wide range of potential applications in evaluating the etiology and efficacy of arsenic.

　　(3) The comparative drug vitamin D causes arterial wall damage, and the formation of sclerosis has long been reported. This animal model showed smooth muscle proliferation, destruction of internal elastic membrane and increase of collagen fibers on the 18th day. By 34 days, smooth muscle cells will grow from the destruction of the internal elastic membrane, and some smooth muscle cells will become foam cells. The whole pathological change process is similar to the pathological changes in As, similar to the previous changes. The pathological processes caused by high-fat foods (such as collagen) are basically the same. Studies have shown that the level of calcium content in the coronary artery wall is closely related to the formation of lipid streaks, fibrous plaques and late As complex plaques in the coronary artery wall. Due to calcium overload, the model established an As model. A large number of vitamins will calcify the arteries, thereby affecting lipid absorption and blood lipid levels. Vitamin D may also impair the integrity of the endothelium of the arterial wall. Plasma lipids invade and damage the tube wall, thereby forming arteriosclerosis.