动物模型,肺心病 z-bo 2020-08-06 600

　　(1) Reproduction method Experimental rabbits use 1% FeCl3 aqueous solution to slowly inject 1~1.5ml through ear vein, and spray 0.5ml of cadmium chloride aqueous solution to the rabbit’s throat at the same time every 3 days. Cor pulmonale will develop after 45 days. model. Or use male Wistar rats to replicate the rat pulmonary hypertension model of hypoxia combined with intravenous FeCl3. The rats were placed in a hypoxic chamber, and nitrogen was injected into the chamber to reduce the oxygen concentration to 10% within 30 minutes. The CO2 and H2O in the chamber were absorbed by soda lime and anhydrous calcium chloride. Hypoxia is 8 hours a day, 6 days a week. After hypoxia on the 3rd and 6th days of each week, the tail was scrubbed with warm water and routinely disinfected, and 0.6% FeCl3 (dose 0.2ml/100g body weight) was slowly injected through the tail vein. Two to four weeks after modeling, the animals were dissected, and lung histopathological examination was performed, fixed with 10% neutral formaldehyde solution, embedded in paraffin, and routinely prepared. HE staining, light microscope observation. In addition, the pathological changes of the pulmonary artery were observed by transmission electron microscope. Light microscope observation revealed that right ventricle hypertrophy, pulmonary artery smooth muscle hypertrophy and vascular lumen stenosis after 32 weeks of hypoxia and FeCl. At 4 weeks, the pulmonary vascular smooth muscle was obviously proliferated and hypertrophy, and the alveoli were enlarged and ruptured, showing emphysema, and there was inflammatory cell infiltration in the interstitium. Transmission electron microscope observation of hypoxia superimposed on FeCl 34 weeks showed endothelial cell swelling, mitochondria swelling, cristae dissolved and blurred, endothelial cells separated from basement membrane, cell connection relaxation; vascular endothelial peeling, subintimal tissue exposed, subintima and elastic fibers deformed , Platelet aggregation, microthrombosis.

　　(2) Model characteristics The modeling agent in this model is generally damaging to the vascular intima, so it is not specific to the pulmonary blood vessels. Therefore, it causes pulmonary blood vessel damage and inflammation as well as other major diseases in the body. Damage to the lining of blood vessels. However, rats in the hypoxia superimposed FeCl3 group showed pulmonary artery endothelial cell shedding, exposure of subintimal tissue, vascular smooth muscle cell proliferation and a large number of inflammatory cell infiltration, which is a pulmonary artery that can better reflect the role of hypoxia and inflammatory factors in the pathogenesis of pulmonary hypertension. High-pressure animal model. Moreover, FeCl3 as a commonly used chemical reagent has the advantages of being cheap and easy to obtain, and less toxic to the human body, so it is also a commonly used animal model.

　　(3) Comparative medicine The possible mechanism of intravenous FeCl3 causing pulmonary hypertension is: ① Repeated violent spasm of blood vessels leads to muscular layer hypertrophy. ② Damage to the vascular endothelium causes the intimal hyperplasia, narrowing the lumen and increasing resistance. ③Promote thrombosis in small blood vessels and capillaries, gas exchange barriers, and lower oxygen partial pressure. ④ Increased blood coagulation and increased blood flow resistance. Hypoxia combined with intravenous injection of FeCl3 can cause pulmonary vascular endothelial cell damage, smooth muscle thickening, inflammatory cell infiltration, microthrombosis and other disease-related pathological changes.