股骨头缺血性坏死介入治疗的实验研究

目的:探讨激素性股骨头缺血性坏死发病机理及介入治疗效果。方法:成年新西兰大白兔40只随机分成三组。A组为空白对照组;B组为激素组,给予臀部肌肉注射地塞米松2.5mg/kg,每周3次,连续给药20周;C组为激素+治疗组,在20周时从双侧股动脉灌注复方丹参各5ml、蝶脉灵各1.0ml/kg。24周全部处死动物,观察X线平片、血管造影及股骨头病理学变化。结果A组X线片全程无变化,B组、C组20周时见股骨头内密度局限性减低,部分可见大小不等的囊状透光区。24周时B组股骨头密度减低持续存在,囊状透光区有扩大倾向。而C组股骨头骨坏死有部分修复。血管造影显示三组动物髋关节区血管分布无差异。光镜下B组见典型的骨坏死灶及软骨下区较多空缺骨陷凹,髓腔内基本为脂肪细胞所取代,与A组差异明显(P<0.01)。C组与B组相比较却减轻(P<0.05),但仍未恢复至A组水平(P<0.05)。结论:髓腔内脂肪细胞增生肥大造成填塞而引起微循环障碍是导致股骨头缺血性坏死的重要病理因素。血管造影检查对ANFH诊断无特异性,从股骨头供血动脉快速注入高浓度扩血管和改善微循环药物,能疏通股骨头的营养血管,防止骨坏死进一步恶化,有利于坏死的骨质修复。

The experimental study of interventional therapy for avascular necrosis of the femoral head

Objective To study the pathogensis and interventional therapy for avascular necrosis of the femoral head(ANFH) caused by steroid. Method Forty new zealand adult rabbits were randomly divided into three groups. Group A served as control, group B received intramuscular injections of dexamethanose at a dose of 2.5 mg/kg three times a week for 20 weeks. In addition to regular dexamethasone injection, Fu Fang Dan Shen was given at a dose of 5ml through bilateral femoral artery in the 20th week, and Die Mai Ling was also employed at a dose of 1.0 mg/kg in group C. All survival animals were killed in order to observe X-ray plain film, angiography and pathological change of femoral head in the 24th week. Results Radiographs were no change all the time in Group A. In Group B and C, localized low density was showed in the region of the femoral head, some part of which was displayed cystic change. In Group B, lower density region still existed and cystic change tended to extend by the 24th week. However, osteonecrosis had partial restoration in Group C. Angiography showed no obvious abnormality of the hip joint in three groups. There were typical osteonecrosis and an increase in number of vacant bony lacunae in the subchrondral region and fatty cell took up considerable space in marrow cavity in group B. There were notably distinction compared with group A(P<0.01). Group C had a significant improvement compared with group B (P<0.05), but it still didn't reach the standards like Group A(P<0.05). Conclusion The fatty cell tamponade owing to excess and hypertrophy, which led to microcirculation disorder in the medullary cavity ,was an important pathological factors causing ANFH. Examination of angiography lack specificity for the diagnosis of ANFH. Rapid perfusion of drugs that ameliorated microcirculation at high concentration from supplying arteries of the femoral head had the effect to dredge the nutritional blood vessels, prevented osteonecrosis from progressing and promoted restoration of necrotic bone.