动物模型,股骨头缺血性坏死 z-bo 2020-08-08 429

　　1 Liquid nitrogen freezing method

　　(1) Method of replication The experimental dog was anesthetized by intravenous injection of sodium pentobarbital at a dose of 30 mg/kg body weight. A posterolateral incision was made on one hind limb of the animal, and the proximal femur was bluntly separated and exposed. The round ligament was cut to make the femur Dislocation free. Wrap the surrounding soft tissues with sterile gauze and cotton pads to prevent frostbite. Instill liquid nitrogen on the femoral head for about 2 minutes, refill the femoral head, and suture the joint capsule to maintain joint stability.

　　(2) Model characteristics The main manifestations of the model under the animal microscope are bone marrow tissue edema and hematopoietic cell coagulation necrosis on the 1st to 3rd day after the operation; the necrosis of bone cells and osteoblasts disappears, a large number of red blood cells in the medullary cavity leak out, and the blood vessels There is thrombosis and hemosiderin deposits; the trabecular bone becomes thinner, fractured, and disintegrated on the 12th postoperative day, and inflammation occurs; the trabecular bone is further disintegrated on the 19th to 33rd postoperative day, and the fracture shows granular changes, small blood vessels and fibers The mother cell grows into the necrotic zone, new bone is formed, interstitial reaction, and collagen fibers are gradually formed.

　　(3) Comparative medicine Human avascular necrosis of the femoral head is divided into two types: traumatic and non-traumatic. The pathogenesis of the former is clear, and the pathogenesis of the latter is not fully understood. The basic pathological changes of all avascular necrosis of the femoral head are the same, that is, bone cell necrosis first, and then repair response. This model is made by liquid nitrogen freezing method, and its lesions are from necrosis to changes in bone marrow during repair. This model reflects the pathological changes of early avascular necrosis of the femoral head, which occurs due to interruption of blood supply and freezing. The initial stage is necrosis of bone cells and bone marrow cells. Edema is caused by venous congestion caused by interruption of blood flow, increased pressure, and tissue fluid leakage after freezing.

　　2 Hormonal method

　　(1) Method of replication The experimental rabbits were first injected with horse serum 10ml/kg body weight, 2 times, 2 weeks apart, 2 weeks after the last injection of horse serum, 40 mg/kg body weight was injected intraperitoneally every day for 3 days. Prednisone.

　　(2) Model features: Empty bone lacunas and intramedullary fat cells in the model animal were seen at 8 weeks of modeling; at 16 weeks, necrotic bone trabecula of the hollow bone lacunas were broken, seizures appeared, and intramedullary fat cells appeared. The bone trabeculae were slender and fractured, the distance between the trabeculae was enlarged, the sequestrum slices were darker, the structure was fuzzy and uneven, and the hematopoietic marrow was replaced by adipose tissue. In each stage, the structure of the vascular wall of the nutrient arterioles is unclear, some blood vessels are filled with mesh fibers, some red thrombosis can be seen, the number of blood vessels is significantly reduced, and there are extensive new and old bleeding areas in the bone marrow. Scanning electron microscopy showed that the collagen fibers on the surface of the bone matrix were disorderly arranged at 8 weeks, and the fibers were widely loosened, and there were very few osteoblasts on the trabecular bone surface; at 16 and 24 weeks, the bone trabecula broke and collapsed, and the collagen fibers on the bone matrix surface were loose. Unbroken. Transmission electron microscopy showed that bone cells were in the stage of degeneration and necrosis at 8 weeks. The degeneration of bone cells mainly showed swelling of the organelles in the cytoplasm, the structure of the organelles was unclear, or the structure of the organ membrane disappeared, and the necrotic bone cells mainly showed pyknosis of the nucleus. , Heterochromatin concentration, nuclear fragmentation, cell disintegration, occasional degeneration bone cells containing lipid droplets; there are still more degeneration and necrotic bone cells at 16 weeks, and the number of degeneration bone cells containing lipid droplets increases; at 24 weeks Most of them are osteocytes in the degenerative necrosis stage, the cell volume occupies the entire bone lacuna, huge lipid droplets are visible in the cell, the nucleus is squeezed to one side to form a crescent shape, heterochromatin is concentrated, and nuclear pyknosis, fragmentation, and disintegration can be seen , Fat droplets can be seen in the bone tubules.

　　(3) Comparative Medicine Avascular necrosis of the femoral head caused by adrenal cortex hormones accounts for the majority of non-traumatic osteonecrosis, mainly involving young and middle-aged people, and mostly bilateral, which seriously affects the quality of life of patients. The clinical manifestations of animal models of avascular necrosis of the femoral head induced by hormones in the past are quite different from humans. This model first uses horse serum to induce type III allergies in rabbits. The antigen-antibody complex deposits on the blood vessel wall to cause hypersensitivity vasculitis. At the same time, glucocorticoids are used to inhibit the synthesis of collagen and elastic fibers, which damages the existing vasculitis. Blood vessels can aggravate the contraction of blood vessels, promote platelet aggregation, inflammatory proliferation of endothelial cells, breakage of elastic fibers in the middle layer, which can lead to rupture or embolism of small arteries, and intramedullary hemorrhage.