酒精中毒导致股骨头缺血性坏死发病机理的研究(摘要) |
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引用本文: | 王义生 毛克亚. 酒精中毒导致股骨头缺血性坏死发病机理的研究(摘要)[J]. 河南医学研究, 1997, 6(4): 318-319 |
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作者姓名: | 王义生 毛克亚 |
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作者单位: | 河南医科大学第一附属医院骨科,河南医科大学生化教研室 |
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摘 要: | 目的:探讨酒精中毒导致股骨头缺血性坏死的发病机理。方法:取健康新西兰种家兔80只,随机分为实验组和对照组,每组40只。采用灌胃法,实验组给予烈性酒(含乙醇45%)10ml/kg·d,对照组给予10%的葡萄糖溶液10ml/kg·d。两组动物在实验第1、2、3、6月时分批处死,定期观察其血清学变化和肝脏、股骨头的组织学改变。结果:和对照组相比,实验组结果显示血清LPO、GGT、AST、ALT、TG和CHO升高,SOD活性降低,肝细胞脂肪变性,股骨头髓内脂肪细胞增殖肥大,空骨陷窝百分比升高,骨小梁变细、稀疏,面积分数降低,透射电镜下见股骨头软骨下骨细胞内出现异常增多的脂质沉积。结论:提示过量饮酒可导致股骨头缺血性坏死。
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关 键 词: | 股骨头坏死;酒精中毒;脂质沉积;脂肪变性 |
Experimental Study on the Pathogenesis of Alcoholism induced Avascular Necrosis of the Femoral Head(Abstract) |
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Abstract: | $$$$ Wang Yi sheng Mao Ke ya Li Yue bai 1 et al (The First Affiliated Hospital of Henan Medical University, Zhengzhou 450003) Abstract Objective: In recent years,the clinical report on the alcoholism induced avasculal necrosis of the femoral head(ANFH) increased .Because this disease often appears in adults and easilly causes disabilities,ours health is seriously threatened by ANFH .But there is no animals experimental study being reported about stong wine intake induced ANFH in the world till now.Its pathogenesis is not clear.By pouring into stomach in this study,a high dose of stong wine was administered to rabbits to produce alcoholism induced ANFH animals model. Series abnomal changes of experimental animals were observed to revel the pathogenesis,which would give a science basis to clinically prevent and treat alcoholism induced ANFH.Methods: In this study,80 New Zealand rabbits were randomly divided into experimental group and control group,there being 40 animals in each one respectively. By pouring into stomach,the experimental group were adiministered 10 ml/kg·d wine, which contains 45% ethanol,and the control group were given the same dose of 10% glucose solution.The animals from two groups were sacrificed in batches in the 1th,2th,3th and 6th monthes periodically after treatment.The changes of serology and histology of liver and femoral head were studied.Results: Comparied with the same time control groups,the experimental groups results showed increased levels of serum lipid peroxides(LPO),gamma glutamyl transferase(GGT), and triglycerid(TG) in the second month,aspartate amino transferase(AST) and cholesterol(CHO)in the third month,alanine amino transferase(ALT)in the sixth month after treatment (P<0.05).Serum superoxide dismutase(SOD) lever reduced in the second month. NO histological changes were observed in the control animals. Wherears the liver of experimental animals showed a fat degeneration in third month,which mainly focused on the center of hepatis lobuli and was more signifisant in the sixth month.Histological of the experimental animalsfemoral head changes mainly focused on the subchondral region.Diminished hemotopoiesis and hytrophied fat were observed. The percentage of empty osteocyte lacuae increased in the second month(P<0.05).The number and size of the marrow fat increased,and the diameter of the biggest marrow fat cell enlarged in the third month(P<0.05), which was more significant in the sixth month.The trabeculace became thin and sparse,and its area fraction reduced in the sixth month. The intracell lipid droplets were observed and nucleus were compressed aside becoming pyknosis and concentrated in the sixth month.When the subchondral osteocytes were examinedb electron microscope,abnomally increased intracellar fat deposits were seen as low electric density.Some osteocyte became pyknosis,and the empty lacuaes was seen.Conclusion: All of these results suggested that a high dose of stong wine being administered to rabbits produce an animals model of ANFH.Excessive intake of stong wine can poroduce:①aberration metabolism of lipid;②hyperlipemia and fatty metamophorsis in the live;③hypertrophic fat cell in bone marrow of femoral head;④fat degeneration of subchondral osteocyte;⑤thin and sparse trabecular and osteopenia.Due to these synthesis effect,ANFH would be resulted in at last. |
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Keywords: | alcoholism necrosis of femoral head fatty degeneration lipid deposit |
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