疾病动物模型,化脓性心包炎 z-bio 2021-03-17 288

　　(1) Breeding method New Zealand rabbits weighing 2.0-2.5 kg, fixed on their back, local infiltration anesthesia with 1% procaine hydrochloride, aseptic surgery, incision in the chest, ribs, ligation, and pericardial exposure area. Under the xiphoid process, penetrate the pericardial cavity with a 7-gauge needle percutaneously to the apex of the heart, and inject 1000,000,000/ml penicillin-sensitive Staphylococcus aureus solution or 1ml/kg saline. Suture the incision. Twenty-one days after the operation, all animals were killed by anesthesia and bloodletting. For pathological examination, three full-thickness myocardium, one liver and one lung tissue, and one pericardium were removed from the apex of the right ventricle. Standardization and quantification of thickening of pericardial purulent adhesions. According to the surface of the heart, it is divided into four areas: the apex of the heart, the left heart (left atrium, left ventricle), the right heart and the roots of the great blood vessels. Each area is determined by the following criteria to determine the degree of thickening. Each area of the pericardium (the grade number is a quantitative number). Grade 0: Normal pericardium. The pericardium is thin and transparent. There is no adhesion between the pericardium and myocardium. The pericardium and the superficial blood vessels and vasculature are clearly visible through the pericardium. Level 1: There are scattered adhesions. There is a small amount of purulent substance in the pericardium and myocardium, the adhesion area, the vascular network is not visible through the pericardium, but the myocardium is still visible; Grade 2: The pericardium is obviously thicker with a lot of pus, and no pericardial pus is visible from the pericardium. And superficial blood vessels. There are many highly dilated blood vessels on the surface of the pericardium. Observe under an optical microscope: fix the myocardial specimen with formaldehyde-sucrose solution, and then HE stain to observe the pathological changes of the pericardium and myocardium. Liver and lung tissues were fixed with formaldehyde. Observe the pathological changes of the liver and lungs. ATPase staining (calcium-cobalt method) to observe the pathological changes of the myocardium. The grade refers to the quantitative number of the Nilest method. Grade 0: Normal myocardium, myocardial fibers are arranged neatly, the stripes are clear, the ATPase activity is strong, and the cell staining is deep and even. Level 1: Close to level 0, the myocardial fibers are still clean, the stripes are clear, the ATPase activity is strong, and the cell staining is deep and uniform. Grade 2: Myocardium is slightly damaged, myocardial fibers are arranged randomly, stripes are covered, ATPase activity is reduced, and cells are slightly stained. Grade 3: Myocardium is damaged, myocardial fibers are misaligned, stripes are obscured, ATPase activity is significantly reduced, and cells may be slightly stained or even unstained. Observation with electron microscope: fix the myocardial specimen with glutaraldehyde, embed it in epoxy resin 618, make ultrathin section (thickness 60m), double stain with heavy metal salt, uranium and lead, and observe with electron microscope. I took a picture. Observe changes in myofibrils, cells, nasal disc, nuclear membrane, sarcoplasmic reticulum, mitochondria, glycogen, etc.

　　(2) The characteristics of the model① are similar to those of human diseases. ②The disease has a certain progression. In other words, there is obviously a stage. ③The formation rate is high and the mortality rate is low. (4) The modeling method is simple and easy to implement. ⑤There are many sources of animals and the price is low. (3) Comparative medicine In this experimental model, the pericardium is used to expose the pleural cavity without damage, and a solution of Staphylococcus aureus sensitive to penicillin is directly injected into the pericardial cavity to purify the pericardium, and a flame model is established. Twenty-one days after the operation, the pericardium of the model animal was visually observed to be significantly thickened, with scattered bleeding points, and a large amount of pus and pus coating between the pericardium and the heart wall. Observation under an optical microscope showed that there were granulation tissue growth, myocardial atrophy, inflammatory cell infiltration, myofilament destruction, hepatocyte granulation degeneration and liver congestion in the pericardium. Pulmonary congestion with pleural effusion. Myocardial ATPase staining showed that the ATPase activity was reduced, the staining was uneven, and the color was light or colored. Disordered placement of muscle fibers and other changes. Electron microscope observation revealed that the muscle filaments area lost sarcoplasm, glycogen was reduced, muscle filaments were destroyed, coagulation became more serious, and some muscle cells contracted rigidly. Some nuclei are swollen. The nucleus is thin, and the myocardial cell disc is scattered and broken. Mitochondria seem to have varying degrees of swelling, matrix loss, blank areas, and sometimes rupture. Lymphocytes and macrophages infiltrate between muscle cells. This model can simulate the pathological development process of purulent pericarditis. This is very similar to the clinical pathophysiology and pathological changes of purulent pericarditis.