脂肪栓塞,动物模型 z-bo 2022-02-06 437

　　(1) Replication method Scrap the long bone marrow of the extremities of the allogeneic experimental dog, incubate it in a 37℃ incubator for 30min, centrifuge at 3000r/min for 10min, the supernatant is the bone marrow fat, and keep it in the refrigerator at -80℃ for later use. Choose healthy mongrel dogs, male or female, weighing 15-18kg. After the frozen bone marrow fat was rewarmed in a water bath to 37°C, it was slowly injected through the canine femoral vein at a dose of 0.7 ml/kg body weight to cause fat embolism syndrome. Observation time is 48h. Observation indicators include: before bone marrow fat injection (0h) and 4, 12, 24, 48 h after injection, heparin anticoagulated femoral arterial blood was drawn, and arterial blood oxygen partial pressure was measured; before bone marrow fat injection (0h) and after injection 4 At 12, 24, and 48 hours, peripheral venous blood was drawn for platelet count and platelet aggregation test; 48 hours after embolization, the animals were sacrificed, lung tissue was taken for gross specimen observation, frozen section oil red O fat staining, paraffin section HE staining, and electron microscope observation. After fat embolism, platelets progressively decrease with the decrease of arterial oxygen partial pressure; platelet aggregation rate increases early and decreases significantly after 24 hours; pathological examination of lung tissue damage is serious: ① Gross examination: lung tissue congestion and edema, massive hemorrhagic Infarction, showing liver-like changes. ②Frozen sections of lung tissue were stained with oil red O: red lipid droplets were seen in the small blood vessels of the lung, the space between lung tissues and the alveolar cavity. ③ Paraffin tissue section, HE staining, light microscope examination: there are lipid droplets attached in the alveolar and pulmonary vessel lumen, pulmonary capillary endothelium swelling, tissue congestion and edema, and inflammatory cells and phagocyte infiltration. ④ Electron microscopy: lipid droplets and platelet aggregation and deformation can be seen in the pulmonary microvascular cavity, pulmonary vascular endothelial cells swell, basement membrane thickening, alveolar type II epithelial cell proliferation and degeneration, mitochondria, lysosomes, rough endoplasmic reticulum damage.

　　(2) Model characteristics Fat embolism syndrome experimental animal models have many replication methods, usually glycerol, triacylglycerol, free fatty acid, mineral oil, olive oil and allogeneic animal tissue fat are injected intravenously to make the animal suffer from fat embolism. Levy. The disadvantage is that most of the embolics are chemical synthetic agents, which are different from the fat embolism components of clinical fat embolism syndrome, so it is difficult to truly simulate the pathogenesis of clinical fat embolism syndrome. Experimental results show that the embolized fat comes from bone marrow, not adipose tissue, chylomicrons, free fatty acids, etc.

　　(3) Comparative medicine Fat embolism syndrome is a serious complication of trauma and fracture. It is an acute inflammatory process that involves multiple chemical mediators and multiple cellular components and promotes each other. The long bone marrow fat of allogeneic dogs was used as fat embolus to establish an animal model of fat embolism syndrome. The clinical manifestations, hematological examination results, gross specimen observation and histopathological examination of the animals were in line with the clinical fat embolism syndrome. Diagnostic criteria.