【摘要】 目的探讨股动脉药物灌注治疗实验性激素性股骨头坏死的机理。方法新西兰兔48只,耳缘静脉注射50μg/kg大肠杆菌内毒素(LPS),24h后重复,在第2次注射LPS后,臀肌注射甲基强的松龙(MP)3次,每次间隔24h。造模4周后随机分为动脉治疗组:经左侧股动脉注射尿激酶3万u和丹参注射液2ml;静脉治疗组:经耳缘静脉注射尿激酶3万u和丹参注射液2ml;对照组:经股动脉注射生理盐水4ml。在治疗后的1、2、3和4周,对股骨头标本分别进行HE染色、苏丹Ⅲ染色、纤维蛋白血栓染色和VEGF免疫组化染色。计数股骨头软骨下骨的空骨陷窝率、脂栓栓塞率、血栓栓塞率、VEGF阳性成骨细胞率、阳性软骨细胞率和阳性血管率,并进行统计学分析。结果动脉治疗比静脉治疗能更快、更有效的降低空骨陷窝率、脂栓栓塞率和血栓栓塞率,提高VEGF阳性成骨细胞率、阳性软骨细胞率和阳性血管率。结论股动脉灌注治疗股骨头坏死比静脉治疗更快速有效。其机理在于溶解血栓和脂栓,再通已经阻塞的血管,促进VEGF等细胞因子的分泌,从而加速股骨头的再血管化和再骨化进程。更多还原

【Abstract】 Objective To study the therapeutic mechanism of medication p erfusion by femoral artery for the femoral head necrosis induced by glucocortico id experimentally. Methods Forty eight of New Zealand rabbits were used for esta blishing the model of femoral head necrosis. The rabbits were injected 50 μ g/ kg LPS in 24h twice intravenously, and methy prednisolone intramuscularly thre e times. The animals were divided into three groups: arterial group which was pe rfused urokinase 30 thousands units and 2 ml red sage root by left femoral arter y; venous group which was perfused urokinase 30 thousands units and 2 ml red sa ge root by era marginal vein; control group which was perfused normal saline. Mi crovessels ink perfusion and pathological examination were adopted to observed t he changes of the femoral head.The ratio of empty lacuna, fatty embolism, thromb us, VEGF positive osteoblast, chondrocyte and blood vessel in the subchondral pl ate were measured by means of HE, sudanⅢ , PTAH and immunohistochemistry in dif ferent periods (1,2,3,4weeks) after the medication perfusion.Results The treatme nt of urokinase and methyl- prednisolone could reduce the ratio of empty lacuna , fatty embolism, thrombus and increase the ratio of VEGF positive osteoblast, c hondrocyte and blood vessel, but the effects of femoral medication perfusion wer e more efficiency and quickly than vein injection. Conclusion The mechanisms con sist in re passing the blocked vessel by dissolving fatty embolism and thrombu s, accelerating the vascular developing and ossification by promoting the exudat ion of VEGF. [更多还原