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The purpose of the experiment, the rabbits were objects made of rabbit hormone femoral head necrosis model to study the large-scale use of glucocorticoid induced hypercoagulability, hyperlipidemia, thrombophilic state reasons and the pathophysiological mechanisms that lead to avascular necrosis, and femoral head necrosis and hemorheological changes the relationship between, and to further explore the pathogenesis of steroid-induced osteonecrosis. At the same time, the rabbit avascular necrosis of the pathophysiological changes, observe the preventive effect of lipid-lowering drugs on hormone-type femoral head necrosis. Methods 54 healthy adult New Zealand white rabbits, male or female, body weight (3.0 ± 0.3) kg, were randomly divided into three groups, each group of 18. Group A (control group): daily intramuscular injection of normal saline; B group (model group): the marginal ear vein injection 10μg/kg LPS (Escherichia coli endotoxin) and 24 h after gluteal injection of 20mg/kg MPS Amber Sodium (methylprednisolone), a total of three times, each time interval 24h: C group (treatment group): modeling, two weeks after intragastric administration of pravastatin sodium 1.5mg/kg A, group B with an equal volume of distilled water. Each group after treatment the 4,6,8,10,12 week line serum cholesterol, triglycerides, low-density lipoprotein, hemorheology, coagulation, thrombomodulin detection of protein content and application SPSS10.0 for statistical software, the comparison between the two sets of data using t test, P <0.05 as statistically significant difference in the standard of data analysis and processing. Rabbits were sacrificed at 6,8,10,12 weeks femoral head gross specimens, the conventional histopathological sections light microscopy, electron microscopy, and vascular endothelial growth factor (vascular-endothelial-growth-factor VGEF) immunohistochemical staining (MSB) staining of the femoral head microvascular thrombosis, according to the dispersion of the animals in each group shares in empty lacunae or pyknosis bone cells around the necrotic bone tissue as avascular necrosis of the histopathological features standard for determining bone necrosis rate statistics. At 12 weeks, rabbits double hip X ray, MRI examination. Results Compared with group A, group B modeling of serum cholesterol (cholesterol, CHOL), triglycerides (triglyceride, TG), under low shear rate whole blood viscosity, plasma viscosity, erythrocyte aggregation index were significantly higher (P <0.05), C group four weeks after modeling, CHOL, TG than in group A, but with the Franco-Prussian prolonged statin medication time, various indicators of group C is gradually returning to normal after 10 weeks of self-modeling was no significant difference between the two groups; B, C between the two groups, eight weeks after the modeling the C group CHOL, TG decreased gradually, since the model 10 weeks after the start of each index between the two groups were statistically difference ((P <0.05). pathology studies have shown that, compared with the same period in group B and C group femoral head osteonecrosis area significantly reduced trabecular bone density increased significantly reduced the number of fat cells in the femoral head medullary cavity empty bone trap nest ratio decreased. Conclusions (1) through a single small dose of LPS (E. coli endotoxin) joint several large dose MPS (methylprednisolone) modeling, rabbit Hormone avascular necrosis was 88.7 % is a safe and effective production of hormones femoral head necrosis model. (2) application of hormones and E. coli endotoxin model, the femoral head within the microvascular endothelial cells damaged small arteries, bone fracture, embolization; dyslipidemia, serum cholesterol, triglycerides, low-density lipoprotein levels increased formation of hyperlipidemia; elevated whole blood viscosity, plasma viscosity and erythrocyte aggregation index, while coagulation abnormalities, blood hypercoagulable state, blood the rheological change; above factors may lead to bone microcirculation, one of the pathogenesis of avascular necrosis (3) use of pravastatin effectively improve lipid metabolism and lower blood viscosity, may also promote vascular endothelial growth factor production, thereby reducing the formation of microthrombi, prevention of femoral head microcirculation and reduce the incidence of hormone type avascular necrosis.
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