动脉粥样硬化 z-bo 2020-08-06 804

　　(1) Reproduction method Male Wistar rats, weighing 180-200 g, were injected intraperitoneally with vitamin D 600,000 U/kg body weight at one time; and fed with basic feed. 34 days after the injection of vitamin D, the animals were anesthetized with pentobarbital sodium, 1% paraformaldehyde plus 1.25% glutaraldehyde solution 300ml, perfused from the left ventricle by intubation, immediately took the aorta for paraffin section, HE staining and ultrasonography Thin section, observation under light microscope and electron microscope. The smooth muscle cell proliferation of the animal aortic wall is obvious, the cell arrangement is disordered, the structure of the elastic fiber layer is unclear, and the local tube wall protrudes into the lumen to form a typical arteriosclerotic plaque. Under the electron microscope, it can be seen that the aortic subendothelial collagen fiber proliferation and smooth muscle There are a lot of collagen fibers between the cells, and foam cells can be seen under the endothelium. Another method is to gavage the stomach with 3,400,000 U/kg body weight of vitamin D at 0, 24, and 48h, and then feed the standard feed. After intragastric administration of 3.4 million U of vitamin D for 9 weeks, arterial slices showed media edema and calcification, media smooth muscle hyperplasia, intimal injury, and subintimal calcification.

　　(2) Features of the model The one-time intraperitoneal injection of vitamin D to induce atherosclerosis has the advantages of simpler operation, lower cost, shorter time and higher success rate than the previous model of feeding animals with vitamin D to induce atherosclerosis. This model has broad application prospects for the pathogenesis of As and the evaluation of drug efficacy.

　　(3) Comparative medicine Vitamin D has long been reported to cause damage to the arterial wall and the formation of hardening. In this animal model, smooth muscle proliferation, internal elastic membrane rupture, and collagen fibers increased on the 18th day. By 34d, smooth muscle cells penetrated from the internal elastic membrane rupture, and some smooth muscle cells became foam cells. The whole pathological change process is similar to the pathological changes of As. The pathological process induced by high-fat foods such as cholesterol is basically the same. Studies have shown that the level of calcium content in the coronary artery wall is closely related to the formation of coronary artery wall lipid streaks, fibrous plaques and advanced As complex plaques. This model establishes an As model by calcium overload. Large doses of vitamins can cause calcification of arteries, which in turn affects lipid absorption and blood lipid levels; vitamin D can also induce damage to the integrity of the artery wall endothelium, which is beneficial to plasma Lipids invade and damage the wall of the tube, thereby forming arteriosclerosis.