化瘀活骨汤治疗肌骨头缺血坏死的实验研究

研究由川芎、三棱、仙灵脾、骨碎补等药组成的化瘀活骨汤治疗股骨头缺血坏死的作用机理。方法应用于方法造成兔股骨头缺血坏死模型，观察化瘀活化汤对其血液流变学的影响。结果造模三周后，治疗组全血粘度、血浆粘度均明显下降，而红细胞聚集指数则上升，与正常组比较无显著性差异，与股骨头缺血坏死模型组比较差异非常显著；光镜观察发现治疗组６周后骨内微循环及骨坏死等病理改变有明显好转，而模型组骨细胞坏死及骨内微循环障碍仍     

中西医结合治疗激素性股骨头坏死的实验研究

目的　探讨中西医结合治疗激素性股骨头坏死的作用机制。方法　将 40只兔子随机分为对照组、模型组、中药组、介入组和综合组。于治疗后 8周 ,分别进行血液流变学、血脂、股骨头空骨陷窝数测定及观察。结果　中药组和介入组动物血浆和全血粘度、红细胞聚集指数、总胆固醇、甘油三脂和股骨头空骨陷窝率均明显低于模型组 (P <0 0 5)。综合组与模型组比较 ,全血高、中切粘度、红细胞聚集指数和甘油三脂明显降低 ,有显著差异 (P <0 0 1 ) ,与中药组和介入组比较亦有差异 (P <0 0 5) ,全血低切粘度、血浆粘度、总胆固醇降低 ,与模型组比较仍有差异 (P <0 0 5) ,空骨陷窝率较模型组显著降低 (P <0 0 1 )。结论　中药组、介入组和综合组治疗股骨头缺血性坏死 ,均可以降低血脂 ,改善血液循环 ,促进坏死骨修复和新生骨再生 ,其中综合组疗效优于单纯内服中药组及单纯介入治疗组     

伤科接骨片对防治鸡激素性股骨头缺血性坏死的实验研究

目的 :探讨伤科接骨片对激素诱导的鸡股骨头缺血性坏死的防治作用。方法 :45只健康成年三黄鸡随机分为三组 :对照组、模型组和伤科接骨片组 ,模型组和伤科接骨片组采用胸肌注射地塞米松磷酸钠建立激素性股骨头缺血性坏死模型。对照组同一时间经胸肌注射等量生理盐水。 12周后取材 ,测定血液流变学指标和股骨头内PO2值 ,并观测股骨头空骨陷窝率。结果 :造模组股骨头内PO2 值明显下降 ,全血粘度、血浆粘度、红细胞聚集指数明显升高 ,而红细胞变形指数明显下降 ,与对照组比较有显著性差异 (P <0 0 5或P <0 0 1) ,应用伤科接骨片后各项指标明显改善 ,与模型组比较有显著性差异 (P <0 0 5或P <0 0 1) ,空骨陷窝率较模型组显著降低 (P <0 0 1)。结论 :伤科接骨片能够改善股骨头血液流变特性 ,对激素诱导的股骨头缺血性坏死有防治作用。     

复元散对激素性股骨头坏死微循环影响的实验研究

目的 探讨验方复元散对激素性股骨头坏死微循环的影响。方法 40只成年雄性新西兰大白兔随机分为模型组（15只），复元散组（15只）和对照组（10只）。模型组采用臀肌注射醋酸氢化泼尼松（简称激素）建立股骨头骨细胞坏死模型。复元散组按上法注射激素并每日灌服复元散。每隔2周各组分别进行全血粘度、甘油三酯、血清总胆固醇及骨内压测定。结果 模型组全血粘度、甘油三酯、血清总胆固醇及骨内压均明显升高，而复元散组各项指标无明显升高（P＜0．01）。结论 复元散能够改善股骨头微循环，扭转股骨头缺血状态，抑制本病的发生发展。     

激素性股骨头缺血坏死发病机制的实验研究

目的　探讨股骨头缺血坏死的发病机制 ,以冀正确指导临床。方法　 2 4只日本大耳白兔随机分为模型组和对照组。给模型组动物大剂量肌注醋酸泼尼松龙 (8mg/kg) 8周 ,造成股骨头缺血坏死模型。造模开始后第 4周、8周、12周两组动物各取 2只进行光镜和扫描电镜观察 ,并在两组动物中各取 4只测定晨空腹血中一氧化氮、组织型纤溶酶原激活物、纤溶酶原激活物抑制物的含量。结果　与对照组相比 ,模型组股骨头骨质疏松 ,光镜下空骨陷窝数增多 ,脂肪细胞数增多 ,扫描电镜下骨小梁断裂塌陷 ,骨基质表面胶原纤维松解、断裂。模型组动物与对照组相比血浆中一氧化氮、组织型纤溶酶原激活物含量下降 (P <0 0 1) ,纤溶酶原激活物抑制物的含量升高 (P <0 0 1)。结论　激素性股骨头缺血坏死可能与一氧化氮含量及纤溶系统的活性下降有关。     

应用血管内皮生长因子基因治疗股骨头缺血性坏死的实验研究

目的：通过建立犬股骨头缺血坏死模型，探讨应用脱蛋白骨复合转染血管内皮生长因子（vascular endothelial growth factor，VEGF）基因骨髓基质细胞植入治疗股骨头缺血坏死的可行性。方法：实验选取36只成年犬，随机分为3组，每组12只。A组为脱蛋白异体骨复合转染VEGF基因的自体骨髓基质细胞；B组为脱蛋白异体骨复合未转染基因的自体骨髓基质细胞；C组单纯植入脱蛋白骨材料。采用液氮冷冻法制作狗股骨头缺血坏死模型，将细胞骨材料复合物植入缺血坏死股骨头内。应用微循环灌注方法了解股骨头内的血运情况，组织形态学观察坏死股骨头的修复情况，免疫组化方法检测VEGF的表达，骨密度仪测定股骨头的骨密度。结果：A组4周后股骨头内有VEGF表达，12周后股骨头内有大量的树枝状血管生成，大量新骨形成，骨密度增高；B、C组均无VEGF基因表达，B组有部分新骨及血管生成，C组仅见少量类骨质形成，血管再生不明显。结论：利用脱蛋白骨复合转染VEGF基因的骨髓基质细胞可促进新骨形成与血管再生，有利于促进坏死骨的修复。     

股骨头缺血坏死的血液流变学临床研究

目的　探讨创伤性与非创伤性股骨头缺血坏死 (ANFN)患者的血液流变学特性。方法　选取创伤性与非创伤性股骨头缺血坏死患者以及其它骨创伤患者共 3组 ,每组 2 8例 ,进行血液流变学指标检测分析。结果　创伤组和对照组比较 ,血小板、血脂含量、血液流变学指标均无明显差异 (P >0 0 5 )。非创伤组和对照组比较 ,全血低切粘度、血浆纤维蛋白原、甘油三脂明显增高 (P <0 0 1)。结论　血液高粘滞状态与创伤性ANFH无明显关系 ,但是可能参与非创伤性ANFH的发病。它的形成可能与高脂血症有关 ,同时还有其它未知病理因素参与。在临床上对有ANFH危险因素的患者进行血液流变学监测 ,可能起到预警作用     

中药复方骨复生对激素性股骨头缺血坏死家兔TNF-α的影响

目的 :探讨中药复方骨复生治疗激素性股骨头缺血性坏死的机制。方法 :32只日本大耳白兔被随机分为空白对照组 (n =12 ) ,造模组 (n =2 0 )。造模组肌注醋酸泼尼松龙 ( 0 32mg/kg·d) 8周。分别在第 6、8周处死每组动物 2只。 8周后将造模组剩余动物随机分为 2组 :骨复生组 (A组 )及模型组(B组 )。原空白对照组剩余动物组成空白组 (C组 )。A组给予骨复生煎液灌胃 ,B组和C组均给予生理盐水灌胃。治疗 4周后 ,采血测定肿瘤坏死因子 (TNF α)水平。结果 :模型组较空白组TNF α水平明显升高 (P <0 0 0 1) ;而骨复生组较模型组TNF α水平明显降低 (P <0 0 1)。结论 :TNF α水平升高可能是激素性股骨头缺血坏死发病的重要促进因素 ,中药复方骨复生可降低TNF α水平从而治疗激素性股骨头缺血坏死     

血管内皮生长因子基因转染促进股骨头坏死修复

目的　探索治疗股骨头及其它骨缺血性坏死新方法。方法　将血管内皮生长因子真核表达质粒pCD hVEGF1652 0 0 μg与胶原混合植入坏死的兔股骨头内 ,术后 2、4周用免疫组化SABC方法检测血管内皮生长因子 (VEGF)表达情况 ,组织形态学分析术后 2、4周修复区血管生成情况及术后 6、8周股骨头新骨形成情况。结果　术后 2周免疫组化证实基因转染组股骨头内有VEGF表达 ,组织形态学检测发现术后 2、4周转染基因的股骨头内血管生长快于对照组 ,术后 4、8周转染基因股骨头新骨形成多于对照组 ,差异均有显著性(P <0 0 1)。结论　利用VEGF基因转染刺激坏死骨组织内血管再生 ,可促进坏死骨修复 ,为临床治疗骨缺血性坏死提供了新的研究方向     

骨生注射液髓腔内注射治疗激素性股骨头缺血性坏死实验研究

目的:研究骨生注射液骨髓腔内注射治疗激素性股骨头缺血性坏死的作用机制。方法:将30只日本大耳白兔用糖皮质激素造成激素性股骨头缺血性坏死模型,随机分为对照组、模型组、治疗组,每组10只。治疗组在造模成功后采用股骨头骨髓腔内注射骨生注射液治疗,于治疗6周后对三组分别进行血液流变学、股骨头空骨陷窝数测定。结果:在全血高切、中切、低切黏度、血浆黏度、红细胞聚集指数、红细胞压积、纤维蛋白原、红细胞刚性指数和股骨头空骨陷窝率的比较上,治疗组均低于模型组(P<0·05);模型组均高于对照组(P<0·01);治疗组与对照组比较差异有统计学意义(P<0·05)。红细胞变形指数比较,治疗组高于模型组(P<0·05);模型组明显低于对照组(P<0·01);治疗组与对照组比较差异有统计学意义(P<0·05)。结论:骨生注射液采用股骨头骨髓腔内注射给药对实验性激素性股骨头缺血性坏死有治疗作用。     

活血补髓汤对激素性股骨头坏死兔模型血浆内皮四项的影响

目的:研究活血补髓汤对股骨头坏死兔模型血浆内皮四项的影响。方法:贺氏造模法,给模型组、对照组、治疗组各10只家兔臀部肌肉注射地塞米松10mg/kg,每周2次,共4周,正常组注射生理盐水。结果:中药活血补髓汤和仙灵骨葆胶囊均可降低血液内皮素及血栓素的含量,升高血液中前列环素及一氧化氮的含量,活血补髓汤作用更加明显。结论:活血补髓汤对激素干预性股骨头坏死兔有治疗作用。     

Ibandronate for prevention of femoral head deformity after ischemic necrosis of the capital femoral epiphysis in immature pigs

BACKGROUND: Femoral head deformity is the most serious sequela of ischemic necrosis of the immature femoral head. The purpose of this study was to determine if a highly potent antiresorptive agent, ibandronate, can inhibit bone resorption during the repair of the infarcted femoral head and thus alter the repair process. We hypothesized that preservation of the trabecular framework by inhibiting osteoclastic bone resorption would minimize the development of deformity in a piglet model of ischemic necrosis. The effect of ibandronate on long-bone growth was also assessed. METHODS: Ischemic necrosis of the right femoral head was produced in twenty-four piglets by placing a ligature tightly around the femoral neck. The animals were divided into three groups according to whether they received saline solution, prophylactic treatment, or post-ischemia treatment. The contralateral, untreated femoral heads from the animals that had received saline solution served as the normal control group. At eight weeks, the femoral heads were assessed for deformity with radiography and for trabecular bone indices with histomorphometry. Also, the length of femur from the untreated side was measured on the radiographs and compared among the groups. RESULTS: Radiographic assessment showed that the epiphyseal quotient, determined by dividing the maximum height of the osseous epiphysis by the maximum diameter, was better preserved in the prophylactic (p < 0.001) and post-ischemia (p = 0.02) treatment groups than in the group treated with saline solution. Histomorphometric assessment also showed that the trabecular bone indices were better preserved in the prophylactic and the post-ischemia treatment groups than in the group treated with saline solution (p < 0.01). The mean femoral length on the untreated side of the animals treated with ibandronate was reduced compared with the length on the untreated side of the animals that had received saline solution (p 相似文献   

一氧化氮对激素性股骨头缺血坏死治疗的生化研究

目的　分析一氧化氮 (NO)在前凝血状况下诱导实验性激素性股骨头缺血坏死过程中的作用。方法　 36只成年新西兰兔随机分为三组 ,A组 (正常对照组 ) 12只 ;B组 (疾病模型组 ) 12只 ,间隔三周于兔耳缘静脉注射马血清 ,共 2次 ,每次10ml/kg。于第二次注射后 2周 ,腹腔连续 3d注射甲基强的松龙 ,共 3次 ,每天 1次 ,每次 4 0mg/kg,建立激素性股骨头缺血坏死模型 ;C组 (治疗组 ) 12只 ,模型诱导方式同B组 ,模型复制成功后 ,将硝酸甘油作为一氧化氮外源供体 ,采用介入疗法 ,通过微泵导管直接注入双侧股骨头供血动脉内 ,持续泵注药液治疗 2周。三组动物均于实验完成后行心内穿刺抽取全血标本 ,测定血小板α颗粒膜蛋白 (GMP - 14 0 ) ,氧化型低密度脂蛋白 (OX -LDL) ,NO的血浆含量 ,而后处死 ,切取双侧股骨头行HE染色 ,光镜下观察病理改变 ,统计空骨陷窝率和软骨下区血管数 ,进行组间t检验。结果　A、C组血浆OX -LDL和GMP - 14 0水平明显低于B组 ,而血浆NO水平明显高于B组。C组空骨陷窝率及软骨下区血管数虽未完全达到A组正常水平 ,但较B组有明显改变。结论　NO生成减少导致的OX -LDL合成增多是引发激素性股骨头缺血坏死过程中系统血管内凝血的重要环节 ,以一氧化氮供体作为药物 ,采用介入疗法治疗激素性股骨头缺     

Peripheral Blood Stem Cell Transplantation for Ischemic Femoral Head Necrosis

Background

Avascular necrosis of the femoral head (ANFH) is a highly mutilating disease. There is no effective way to treat femoral head ischemia. This study was designed to show the curative effects of peripheral blood stem cell transplantation to induce vascular regeneration and improve ischemic femoral head necrosis in rabbits.

Methods

Twenty New Zealand white rabbits underwent ischemic femoral head necrosis in both hindlimbs using liquid-nitrogen refrigeration. One cohort of rats was intraperitoneally injected with granulocyte-specific colony-stimulating factor (250 μg/kg/d), and control animals received equivalent saline solution. The right side was used as the transplantation group and the left as the control. After separation of peripheral blood, a stem cell suspension was poured into the right femoral artery and saline solution into the left femoral artery.

Results

At 4 weeks after peripheral stem cell transplantation, standing ability and activity of the the transplanted right hindlimb were remarkably improved, but there were no obvious changes in the control limbs. The experimental rabbits underwent arteriography of bilateral femoral heads, which indicated increased and thickened blood supply to the transplanted right hindlimb compared with the left control.

Conclusion

Peripheral blood stem cell transplantation improved ischemic femoral head necrosis.     

Study of rotating permanent magnetic field to treat steroid-induced osteonecrosis of femoral head

Sixty New Zealand rabbit models with steroid-induced necrosis of femoral head were exposed to a rotating permanent magnetic field (RPMF) (group A1-2 h/d for one month and group A2-2 h/d for two months), and the changes of femoral head, blood viscosity, serum cholesterol, triglyceride, and pressure within the hip joint cavity were measured and statistically analysed compared to that of control group (B1 and B2) and sham group (C1 and C2). After RPMF treatment, the osteogenesis regeneration of the necrotic femoral head was markedly improved, as was shown by micro-CT. Blood viscosity, serum cholesterol, triglyceride, and pressure in the hip joint cavity were found significantly reduced. RPMF could affect various critical aspects in the course of femoral head necrosis, which will be a promising measure in the prevention and treatment of steroid-induced necrosis of femoral head, especially in the early stage.     

带血管蒂髂骨瓣移植联合活血补肾汤治疗股骨头缺血性坏死的临床研究

目的 观察带血管蒂髂骨瓣移植联合中医活血补肾汤治疗国际骨循环研究学会(ARCO)Ⅱ～Ⅲ期股骨头缺血性坏死患者的Harris评分及X线片改善情况,以验证其治疗优势.方法 40例(49髋)ARCO Ⅱ～Ⅲ期股骨头缺血坏死患者随机分为两组,治疗组22例(28髋)采用带血管蒂髂骨瓣移植治疗,2周后服用活血补肾汤3个疗程;对照组18例(21髋)采用单纯带血管蒂髂骨瓣移植治疗.观察两组术后Harris评分及X线片改善情况.结果 术后18个月治疗组Harris评分及X线片改善情况,均优于对照组.结论 带血管蒂髂骨瓣移植联合活血补肾汤治疗股骨头缺血性坏死的效果明显优于单纯带血管蒂髂骨瓣移植,中药活血补肾汤在缓解患者症状和改善功能方面有明显的作用.     

活血化瘀中药对激素性股骨头缺血坏死模鼠TGF-β1表达的实验研究

目的：观察活血化瘀中药对激素性股骨头缺血性坏死大鼠转化生长因子β1（TGF-β1）表达的影响,进一步探讨其防治激素性股骨头坏死的作用机制。方法：采用清洁级SD大鼠40只,随机分为空白组4只和模型组36只．模型组每周2次腹腔注射醋酸泼尼松龙24．5mg／kg,经6周诱导出早期激素性股骨头缺血坏死的模型,空白组每周2次腹腔注射同等剂量的生理盐水。6周后处死空白组4只和模型组4只,进行光、电镜观察,确定造模成功。随后将其余32只模型组大鼠再随机分为治疗组16只和对照组16只,分别灌服桃红四物汤和生理盐水,于灌胃后第6、8周检测血清中TGF-β1的含量;检测股骨头局部TGF-β1mRNA的转录及股骨头局部TGF-β1的表达。结果：①图像分析仪分析：治疗组股骨头局部TGF—β1较对照组表达明显增强,两组有明显差异（P〈0．01）。②血清TGF-β1含量检测：治疗组血清中TGF-β1的表达增强,与对照组相比有明显差异（P〈0．01）。③股骨头局部TGF-β1 mRNA的转录：治疗组在第6周时表达即增强,在第8周时表达又降低,而对照组在第6周时表达减少,在第8周时未检测到TGF-β1 mRNA的表达,两组有明显差异（P〈0．05,P〈0．01）。结论：活血化瘀中药可促进激素性股骨头缺血坏死模鼠股骨头局部TGF-β1 mRNA的转录水平以及股骨头局部TGF-β1的表达,促进坏死股骨头的修复。     

Upregulation of VEGF in Subchondral Bone of Necrotic Femoral Heads in Rabbits with Use of Extracorporeal Shock Waves

Extracorporeal shock wave treatment appears to be effective in patients with avascular necrosis of the femoral head. However, the pathway of biological events whereby this is accomplished has not been fully elucidated. The purpose of this study was to investigate the effect of extracorporeal shock waves on vascular endothelial growth factor (VEGF) expression in necrotic femoral heads of rabbits. VEGF expression was assessed by immunohistochemistry, quantitative real-time PCR, and Western blot analysis. The degree of angiogenesis was also assessed, as determined by the microvessel density (MVD), the assessment of which was based on CD31-expressing vessels. Bilateral avascular necrosis of femoral heads was induced with methylprednisolone and lipopolysaccharide in 30 New Zealand rabbits. 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. Western blot analysis and real-time PCR showed that shock wave therapy significantly increased VEGF protein and mRNA expression, respectively, in the subchondral bone of the treated necrotic femoral heads. Compared with the contralateral control without shock wave treatment, the VEGF mRNA expression levels increased to a peak at 2 weeks after the shock wave treatment and remained high for 8 weeks, then declined at 12 weeks, whereas the VEGF protein expression levels increased to a peak at 4 weeks after the shock wave treatment and remained high for 12 weeks. The immunostaining of VEGF was weak in the control group, and the immunoreactivity level in the shock-wave-treated group increased at 4 weeks and persisted for 12 weeks. The most intensive VEGF immunoreactivity was observed in the proliferative zone above the necrotic zone. At 4, 8, and 12 weeks after the shock wave treatment, MVD in subchondral bone from treated femoral heads was significantly higher than that in subchondral bone from untreated femoral heads. These data clearly show that extracorporeal shock waves can significantly upregulate the expression of VEGF. The upregulation of VEGF may play a role in inducing the ingrowth of neovascularization and in improving the blood supply to the femoral head.