体外冲击波对兔缺血坏死股骨头血管内皮生长因子表达的研究

目的观察体外冲击波疗法(ESWT)对兔缺血坏死股骨头中血管内皮生长因子(VEGF)表达及毛细血管增生的影响。方法选取体质量3~4 kg健康新西兰大白兔30只,采用脂多糖和甲泼尼龙制造股骨头缺血坏死模型,每只兔子左股骨头接受冲击波治疗,设为实验组,右股骨头不做任何处理,设为对照组。在冲击波治疗后1、2、4、8、12周处死动物取双侧股骨头通过苏木素-伊红(HE)染色观察股骨头愈合的病理改变,免疫组织化学观察VEGF表达的改变,毛细血管密度(MVD)观察新生毛细血管含量。结果实验组股骨头VEGF在ESWT治疗后第2周开始表达,第4周达到高峰,第12周仍很高,VEGF表达最强的区域在坏死后增殖区,对照组虽有VEGF表达,但数量较实验组明显减少。在ESWT治疗后4、8、12周,实验组股骨头MVD显著高于对照组。结论ESWT可以促进兔缺血坏死股骨头VEGF的表达,进而促进毛细血管增生,增加坏死股骨头的血供。

Expression of VEGF in avascular necrosis of femoral heads in rabbits with use of extracorporeal shock waves

Objective To investigate the effect of extracorporeal shock waves on vascular endothelial growth factor(VEGF) expression and angiogenesis in avascular necrosis of femoral heads of rabbits.Methods Thirty New Zealand white rabbits with body weight ranging from 3.0 to 4.0 kg were used in this study.Avascular necrosis of femoral heads was induced with methylprednisolone and lipopolysaccharide.The left limb(the study side) received shock wave therapy to the femoral head.The right limb(the control side) received no shock wave therapy.Biopsies of the femoral heads were performed at 1,2,4,8 and 12 weeks.Hematoxylin-eosin stain was used to assess the pathological change of avascular necrosis of femoral heads.VEGF expression was assessed by immunohistochemistry.The degree of angiogenesis was determined by the microvessel density(MVD),the assessment of which was based on CD31-expressing vessels. Results Compared with the contralateral control without shock wave treatment,the immunoreactivity level in the shock-wave-treated group started to increase at 2 weeks,increased to peak at 4 weeks and persisted for 12 weeks.The most intensive VEGF immunoreactivity was observed in the proliferative zone above the necrotic zone.The immunostaining of VEGF was weak in the control group.At 4,8,and 12 weeks after the shock wave treatment,MVD from treated femoral heads was significantly higher than that in subchondral bone from untreated femoral heads.Conclusion Extracorporeal shock waves can significantly upregulate the expression of VEGF,induce the ingrowth of neovascularization and improve the blood supply to the avascular necrosis of femoral head.