电针督脉不同穴组织促进大鼠脊髓恢复作用的对比研究
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摘要
本论文分文献综述和实验研究两部分。
     第一部分文献综述
     文献综述共三篇。第一篇为针灸对脊髓损伤作用的临床和实验研究概况。第二篇介绍了自由基在脊髓损伤研究中的作用综述。第三篇介绍了回顾了近年来国内外脊髓损伤(SCI)研究中动物模型的选择和应用。
     第二部分动物实验
     目的:针灸对于治疗脊髓损伤所造成截瘫的恢复、缓解肢体痉挛、减轻截瘫性疼痛等方面都有很好的疗效,在临床上被广泛使用。查阅近20年针灸治疗脊髓损伤的相关文献发现:临床上治疗急性脊髓损伤基本上都会用到督脉穴位,按应用频度排序由高到低依次为:受损伤的脊髓节段上方和下方的督脉穴位、“大椎”、“百会”、“命门”、“风府”、“筋缩”等。但在督脉具体取穴上没有以实验室研究为依据的。本课题拟用动物实验的方法来筛选和确定治疗急性脊髓损伤疗效最佳的督脉穴组,以期为临床上治疗急性脊髓损伤在督脉取穴方面提供一定的实验依据。
     方法:将50只SD大鼠大鼠随机分为空白组、模型组、电针I组(取脊髓损伤节段上下方两个脊髓节段的督脉穴位)、电针II组(取“大椎”和“命门”)、药物组(甲基强的松龙)共五组。用改良Allen’s打击法制成脊髓损伤模型,损伤24h后取材。(1)运动联合计分法(CBS)综合评定大鼠脊髓损伤后的神经功能;(2)测定损伤后局部组织SOD含量;(3)测定损伤后局部组织MDA含量。
     结果:
     CBS计分:
     1、术后2h:
     ①与模型组比较,电针Ⅱ组、电针Ⅰ组和药物组与之差异不显著(P>0.05)。
     ②与药物组比较,电针Ⅰ组和电针Ⅱ组与之差异不显著(P>0.05)。
     ③与电针Ⅰ组比较,电针Ⅱ组与之差异不显著(P>0.05)。
     2、术后24h:
     ①与模型组比较:电针Ⅱ组的分值下降,并与之有极显著性差异(P<0.01);电针Ⅰ组和药物组与之差异不显著(P>0.05)
     ②与药物组比较:电针Ⅰ组和电针Ⅱ组与之差异不显著(P>0.05)。
     ③与电针Ⅰ组比较:电针Ⅱ组的分值下降,并与之有显著性差异(P<0.05)。
     MDA:损伤脊髓组织MDA含量进行比较
     1、空白组与模型组比较,模型组MDA含量升高,二者有极显著差异(P<0.01)。
     2、各治疗组与模型组比较:电针Ⅰ组、电针Ⅱ组和药物组MDA含量下降,并均与之有极显著差异(P<0.01)。
     3、治疗组组间比较:
     ①与药物组比较,电针Ⅱ组和电针Ⅰ组与之差异不显著(P>0.05)
     ②电针Ⅱ组与电针Ⅰ组比较,二者差异不显著(P>0.05)。
     SOD:损伤脊髓组织SOD含量进行比较。
     1、空白组与模型组比较,模型组SOD含量下降,二者有极显著差异(P<0.01)。
     2、各治疗组与模型组比较,电针Ⅰ组与电针Ⅱ组SOD含量升高,并均与之有极显著差异(P<0.01),药物组与之差异不显著(P>0.05)。
     3、治疗组组间比较:
     ①与药物组比较,电针Ⅱ组SOD含量升高,并与之有显著差异(P<0.05),电针Ⅰ组与之差异不显著(P>0.05)。
     ②电针Ⅱ组与电针Ⅰ组比较差异不显著(P>0.05)。
     结论:实验数据表明,无论是电针治疗组还是药物治疗组,均可使急性脊髓损伤大鼠CBS计分减少,MDA含量降低,SOD含量提高,说明电针和药物均可对急性脊髓损伤均有疗效,其中以电针大椎、命门组疗效显著。故电针大椎、命门这一穴组可使得行为学计分指标下降幅度较大,SOD含量指标提升较大。
The paper consists two parts: literature review and experimental study.
     First Section: Literature Summary
     There are three literature reviews. The first article introduces the clinical andexperimental survey of the acupuncture and moxibustion on the SCI in rats. The second articleis the review of the free radical on the study of the SCI. The third article is review onthe selection and application of animal model in the studies on the spinal cord injury (SCI)of late years at home and abroad.
     Second Section: Experimental Research
     Objective: Acupuncture which is widely used in the clinical has a good effect on therestoration of experimental identification of specific points on the clinical treatment ofthe paraplegia, ease spastic limbs and reduce the pain paraplegia because of the SCI. Afteraccessing to nearly 20 acupuncture treatment of SCI in the literature, we find that clinicaltreatment of SCI basically used Du Meridian Point, and the frequency of application indescending order is Du Meridian Points in the top and bottom of segment,“DU 14”“DU 20”“DU 4”“DU 16”“DU 8”.There is no laboratory research evidence in how to choose theDU Meridian Points. This research will provide a basis for the acupuncture and moxibustionon the SCI.
     Methods: Rats were divided into five groups stochastically: Blank Group, Model Group, EAⅠ(up and down two of the hurt vertebra )Group, EAⅡ(DU14, DU 4)Group and Drug Group. Themodel rats were made a spinal cord contusion by using a modified Allen’s method.(1)Comprehensive evaluation of neural function of SCI rats by CBS .(2) Detect the superoxidedismutase(SOD) content in injury local tissues after injury.(3) Detect themalondialdehyde(MDA) content in injury local tissues after injury.
     CBD: Two hours after the SCI, (1) Compared with the model group, the score of CBS level inEAⅡGroup, EAⅠGroup and Drug group were not differently(P>0.05).(2) Compared with theDrug Group, the score of CBS level in EAⅠgroup and EAⅡwere not differently(P>0.05).(3) Compared with the EAⅠGroup, the score of CBS level in EAⅡGroup was not differently(P>0.05).
     Six hours after the SCI, (1) Compared with the model group, the score of CBS level in EAⅡGroup was extremely significant differently(P<0.01), the score of CBS level in EAⅠGroup and Drug group were not differently(P>0.05).(2) Compared with the Drug Group, thescore of CBS level in EAⅠgroup and EAⅡwere not differently(P>0.05)(3) Compared withthe EAⅠGroup, the score of CBS level in EAⅡGroup was significant differently(P<0.05)MDA: 1.Compared with the blank group, the score in model Group increase and was extremelysignificant differently(P<0.01). 2.Compared with the model group, the score in EAⅠGroup , EAⅡGroup and Drug group were extremely significant differently(P<0.01. 3.Compared withthe Drug group, EAⅡGroup and EAⅠGroup were not differently(P>0.05). Compared with theEAⅠGroup, EAⅡGroup was not significant differently(P>0.05)
     SODSOD: 1.Compared with the blank group, the score in model Group decrease and was extremelysignificant differently(P<0.01). 2.Compared with the model group, the score in EAⅠGroup ,EAⅡGroup were extremely significant differently(P<0.01), Drug group was not differently(P>0.05). 3.Compared with the Drug group, EAⅡGroup was significant differently(P<0.05),EAⅠGroup was not differently(P>0.05). Compared with the EAⅠGroup, EAⅡGroup was notsignificant differently(P>0.05)
     Conclusion: Experimental data show that, whether the EA group or the Drug group, they allcan make the score of CBS decrease, MDA decrease and SOD increase. That means EA group andthe Drug group all have effect on SCI. The effect of EAⅠGroup is better. Soelectroacupuncture treatment in DU14, DU 4 can make the score of CBS decrease more and SODincrease more.
引文
[1] 吴永刚,刘成德,孙忠人,等.针刺对实验性脊髓损伤组织形态学的影响.上海针灸杂志,1999,18(3):33.
    [2] 郝树萍,郭友仁,杨春伯,等.脊髓损伤并发下肢感觉丧失性疼痛的临床研究.中国疼痛医学杂志,1996,2(2):65-71.
    [3] 陈之罡.脊髓损伤常见并发症的中医治疗.中国康复理论与实践,2003,9(2):86-87.
    [4] Skold C, Levi R, Seiger A. Spasticity aftert raumatic spinal cord injury: Nature, severity, and location.Arch Phys Med Rehabil, 1999,80:1548-1557.
    [5] 陈之罡,张进军,王征美,等.督脉电针治疗脊髓损伤下肢痉挛的临床观察.针灸临床杂志,1995,11(6):6-7.
    [6] 汪家琮,周红俊,刘根林,等.韩氏穴位神经刺激仪(HANS)治疗脊髓损伤引起的肌痉挛痛.中国疼痛医学杂志,2000 ,4 (4):217-224.
    [7] 罗非,反复电针对慢性痛的累加治疗作用及其机制的研究.生理科学进展.1996,27(3):241-244
    [8] 宋玉凯.TENS 治疗截瘫神经痛的临床疗效观察.[J].第一届中日脊髓损伤研讨会论文摘要选编(中国部分第一分册),1998,126.
    [9] 黎桃英.电针夹脊穴治疗脊髓损伤的疗效观察.上海针灸杂志,2002,21(5):42.
    [10] 校佰平,徐德艺,屈继宁.截瘫患者心理康复治疗体会.中国康复医学杂志,2000,15(6):371-372.
    [11] 乔鸿飞, 康晓玲. 电针对脊髓损伤合并抑郁症患者免疫功能的影响. 河北医药,2005,27(3):216-217.
    [12] 李惠兰,头针治疗截瘫神经痛疗效观察.中国针灸,2001,21(4):209-210.
    [13] 李观荣,李琼研,陈岚,等.头针治疗外伤性截瘫神经根性疼痛82例.河北中医, 2000, 22(3):208.
    [14] 陈志华.150例外伤性截瘫的针刺治疗与体会[J].天津中医,1989,(5):5.
    [15] 许建鹏,王明久,刘学茹,等.以督脉电针为主治疗脊髓损伤 80 例的临床观察[J].针灸临床杂志,1994,10(6):13-15.
    [16] 熊华,何杨子.电针治疗脊髓损伤17例疗效分析.海南医学19956(2):107-109.
    [17] 张芸.针刺取穴与脊髓损伤恢复的关系探讨.中国中医骨伤科杂志,2002,10(6):58-59.
    [18] 余安胜.督脉电针电场治疗半横断脊髓损伤的实验研究针灸临床杂志,1995(1):24-26.
    [19] 刘树清,胥少汀,孙天胜等,脊髓脉冲电场结合理疗治疗陈旧脊髓不全损伤后运动功能障碍,现代康复,2000(10):1544-1548.
    [20] 盛国滨,唐英.应用齐刺法治疗外伤性截瘫48例.中医药学报2002(1).
    [21] 黎桃英.电针夹脊穴治疗脊髓损伤的疗效观察.上海针灸杂志2002;21(5):42
    [22] 高兵兵,张宁,江红,等.夹脊电针治疗脊髓性截瘫的体感诱发电位(SEP)研究.针灸临床杂志,2005,21(9):23-24.
    [23] 白晔,庄明华,谢泽宇,等.电针辅助治疗对急性不完全性脊髓损伤的疗效.中国康复理论与实践,2005, 11(7):582-583.
    [24] 黄志刚,尤斌.针刺治疗脊髓损伤后尿潴留32例.上海针灸杂志,2002,21(2):31.
    [25] 顾旭东,傅建明,姚云海.电针八髎穴为主治疗脊髓损伤排尿障碍 64 例疗效观察.针灸临床杂志,2005, 21(4):47-48.
    [26] 刘进. 电针治疗脊髓损伤性尿潴溜34例.针灸临床杂志.1997,13(8):31
    [27] 彭享娣,张素洁,司同,等.督脉电针对外伤性截瘫患者尿路功能的改善.中国针灸.增刊:84-87.
    [28] 徐斌.脊髓针为主综合治疗法治疗外伤性截瘫286例疗效观察[J].中国针灸,1990,(2):7-9.
    [29] 郑谅,杨晓光.直接灸结合中药薰洗治疗外伤性截瘫49例.上海针灸杂志,2000,19 (1): 32-33.
    [30] 秦家超.督脉温针治疗截瘫疗效分析.中医外治杂志,2002,11(4):42.
    [31] 刘志良.针灸为主治疗外伤性截瘫224例临床观察.针灸临床杂志,2001, 17(5):25-26.
    [32] 俞昌德,俞兰英,黄宗勖.针灸治疗创伤性排尿障碍临床观察.中国针灸,200 1,21(6):345-346.
    [33] 陈丽贤,段俊峰,詹欣荣,等.电针结合耳针治疗急性脊髓损伤的临床研究.中国康复理论与实践,2005,11(11):934-935.
    [34] 王忠.电针、穴位注射、推拿按摩综合疗法治疗外伤性截瘫 18 例.甘肃中医学院学报, 2002,19(1):52-53.
    [35] 张红,宋霞.新斯的明行足三里穴位注射治疗 32 例外伤性截瘫术后腹胀患者.解放军护理杂志,2003,20(2):77.
    [36] 司同,汪家琮,阎增红,等.针刀松解术与肌松剂药物治疗改善脊髓损伤并发肌痉挛的效果比较.中国临床康复,2005,9(29):32-33.
    [37] 张志英,余安胜,等.电针对脊髓损伤早期 caspase-3 mRNA 及蛋白表达的影响. 解剖学杂志,2002,25(6):548-552.
    [38] 张志英,崔云华,严振国.电针对脊髓损伤后细胞凋亡的影响.中国临床康复,2002,6 (6): 818-819.
    [39] 杨成,李滨,刘同慎,等.电针对脊髓损伤后星形胶质细胞增生的影响.中国针灸,2005,25( 8):569-572.
    [40] 杨成,刘同慎,吴洪华,等.电针对脊髓损伤后少突胶质细胞再髓鞘化的影响.解剖学杂志,2005,28(4):391-394.
    [41] 杨成,赵冬梅,刘同慎.督脉电针治疗脊髓损伤后不同神经营养因子表达的时间窗特征.中国临床康复,2005,9(25):135-137.
    [42] 谌宏鸣,吴良芳,保天然,等.针刺对去部分背根猫脊髓和背根节NGF及NGFmRNA的影响.神经解剖学杂志,2000,16(4):319-322.
    [43] 孙双历,严振国.电针对大鼠脊髓损伤后 CBS 及 HBP 追踪的实验研究.中国中医药科技,2000,7(11):1-2.
    [44] 李连欣,张进禄,周东生,等.电针对实验性脊髓损伤后兴奋性氨基酸含量的影响.中国针灸,2000,20(12):741-742.
    [45] Baba H, Maezawa Y, Imura S, et al. Quantitative analysis of the spinal cord motoneuron under chronic compression :an experimental observation in the mouse. J Neurol,1995,243:490.
    [46] 王新家,孔抗美,齐伟力.针刺对慢性脊髓损伤大鼠神经递质和营养因子表达的影响.中国康复理论与实践,2005,11(2):94-95.
    [47] 杜泽吉,周立人.自由基介导的组织损伤机制.国外医学卫生学分册,1992,2:79283
    [48] 陈亮,甘德坤,马玲,等.男性吸烟者血清 SOD 及 MDA 水平的量化研究.中国自然医学杂志,2004,6(2):69270
    [49] Aydin S, Aral I, Kilic N, et al. The level of antioxidant enzymes, plasmavitamins C and E in cement plant workers. Clin Chim Acta,2004,341 (122):1932198
    [50] 袁青,易玮.针刺对脑梗塞患者体内超氧化物歧化酶,丙二醛的影响[J].针刺研究,2000,25(3):217-219.
    [51] 王光义,蒋乃昌,贺志光.光针对脑梗塞患者血浆 ET - 1、MDA、NO 的影响[J].中国针灸,2001,21(4):241-242.
    [52] 孙忠人,赵英,毕克滨,等.足三里抗衰老作用的实验研究[J].针灸临床杂志,1996,12(2):33.
    [53] 唐照亮,宋小鸽,侯正明,等.艾灸肾俞延缓衰老的实验研究[J].安徽中医学院学报,1999,18(5):53-55.
    [54] 张春红,王舒,赵俊宏,等.针刺对实验性脑缺血大鼠脑组织 SOD、MDA 的影响[J]. 天津中医学院学报,1999,18(4):39-40.
    [55] 赵建新,田元祥,曹刚,等.电针肾俞、膈俞、百会穴对拟血管性痴呆小鼠脑组织SOD 活力、MDA 含量的影响[J].中国中医药科技,2000,7(2):65 - 66.赖新生,王黎,江雪华,等.
    [56] 赖新生等,电针对实验性血管性痴呆大鼠学习记忆及 SOD 和 MDA 的影响[J].中国针灸,2000, (8):497-500.
    [1] 方允中,自由基的基本概念.见: 方允中,李文杰主编,自由基与酶---基础理论及其在生物学与医学中的应用.北京:科学出版社,1989,1~12
    [2] NonhebelDC,WaltonJC.Free-RadicalChemistry:Structure and echanism.Cambridge:Cambridge University Press,1974
    [3] Parson AF.An Introduction to Free Radical Chemistry Oxford:Blackwell Science Ltd.2000
    [4] Fridovich I.Superoxide Dismutase.Meth.Enzymol,1986,58:61~97
    [5] 方允中.生物体内自由基的产生和清除 见:方允中 李文杰主编:自由基与酶――基础理论及其在生物学和医学中的应用 第八章 北京:科学出版社.1989:147~162
    [6] 方允中.生物分子的自由基损伤及其修复或重新合成,第十次中国生物物理学会学术会议论文摘要集 1998
    [7] 夏寿莹.活性氧所致体内DNA损伤及其老化的关系.见: 方允中、郑荣梁、沈文梅主编、自由基生命科学进展,第3集,原子能出版社,北京:1995:99~102
    [8] McCord JM,Keele BB,Fridovich I.An enzyme-based theory of obligate anaerobiosis.The physiological function of superoxide dismutase.Proc Natl Acad Sci USA,1971,68:1024-1027
    [9] Sawyer DE,Van Houten B.Repair of DNA damage in mitochondria.Mutation Res,1999,434:161-176
    [10] Kowaltowski AJ,Vercesi AE.Mitochondria damage induced by conditions of oxidative stress.Free Radic Biol Med,1999,26(3/4):463-471
    [11] Halliwellb,Aruoma OI .dna damage by oxygen-derived species.its mechanism and measurement in mammalian system febs lett,1991,281:9-19
    [12] breen ap,Murphy ja. Reaction of oxyl radiacals with dna.free radic boil med,1995,18:1033-1077
    [13] meneghini r.iron homeostasis,oxidative sress,and dna damage,free radic boil med,1997,23:783-792
    [14] douki h,cadet j.peroxinitrite mediated oxidation of purine bases of nucleosides and isolated dna.free radical res,1996,24:369-380
    [15] Collins ar.oxidative dna damage,antioxidants and cancer.bioessay,1999,21:238-246
    [16] halliwell b. oxygen and nitriogen are pro-carcinogens. damage to dna by reactive oxygen, chlorine and nitrogen species: measurement, mechanism and the effect of nutrition.mutation res,1999,443:37-52
    [17] burcham pc.internal hazards:baseline dna damage by endogenous products of normal metabolism,mutation res.1999,443:11-36
    [18] liebler dc.free-radical defence and repair mechanisms.in:free radical toxicology Wallace kb.ed.taylor-francis,1997:141-171
    [19] starke dw,chen yc.bapna cp,et al.sensitivity of protein sulfhydryl repair enzymes to oxidative stress.free radic boil med,1997,23:373-384
    [20] stadtman er.metal ion-catalyzed oxidationof proteins:biochemical mechanism and biological consequences.free radic boil med,1990,9:315-325
    [21] stadtman er.oxidation of proteins by mixed-fuction oxidation systems:implicaton in protein turnover,aging and neutrophil function.trends biochem sci,1986,11:11-12
    [22] hunt jv,simpson ja,dean rt.hydroperoxide-mediated fragmentation of proteins.biochen j,1988,250:87-93
    [23] amiei a,Levine rl.tsai l,et al.convertion of amino acid residues on proteins and amino acid homopolymers to carbonyl derivatives by metal.catalyzed oxidation reactions.j boil chem.,1989,264:3341-3346
    [24] davies lja,delsignore me.protein damage and degradation by oxygen radicals.j boil chem.,1987,262:514-579
    [25] stadtman er,Barbara sb.free-radical-mediated modification of proteins.in:Wallace kb.ed.free radical toxicology.new york:taylor francis 1997:70-87
    [26] maskos z,ruth jd,koppenol wh,the hydroxylation of tryptophan.arch biochem.biophys,1992,269:514-579
    [27] davies kja,delsignore me,lin sw.protein damage and degradation by oxygen redicals.modification ofamino acids.j boil chem.,1987,223:9902-9907
    [28] 汪吉明,孔抗美,崔华中,等. 电针对脊髓损伤后神经生长相关蛋白GAP-43表达的影响.广东医学,2007, 28 (1):40-41.
    [29] esterbauser h,gebicki j,puhl h,et al.the role of lipid peroxidation and antioxidants in oxidative modification of ldl.free radic boil med,1992,13:341-390
    [30] 庞战军、周玫、陈瑗著.自由基医学研究方法.人民卫生出版社.1990:60-105
    [31] kietzmann d,kahl r,muller m et al.hydrogen peroxide in expired breath condensate of patients with acute respiratory failure and with ards.int care med,1993,19:78-81
    [32] pinsky dj,naka y,chowdhury nc et al.the nitric oxide/cyclic gmp pathway in organ transplantation:critical role in successful lung preservation.proc natl acad sci usa,1994,91:12086-12090
    [33] bacha ea,herre p,murakami s et al.lastiong beneficial effect on short term inhaled nitric oxide on graft function after lung transplantation.j thorac cardiovasc surg,1996,112:590-598
    [34] orancy rm,leszczynska-piziak j,Abramson sb et a.nitric oxide,an endothelial cell relaxation factor,inhibits neutrophil superoxide anion production via a direct action on the nadph oxidase.j clin invest,1992,90:1116-1120
    [35] COLL INSW F. A review and update of experimental and clinical studies of sp inal cord injury [J].Paraplegia,1983,21:204-209
    [36] ALEXANDER G, YAKOVLEV, ALAN I, et al.Mechanisms of neural cell death: imp lications for development of neurop rotective treatment strategies[J].NeuroRx,2004,1(1):5-16
    [37] Sakurai M ,Hayashi T ,Abe K,et al. Delayed and selective motor neu-ron death after transient spinal cord ischemia : a role of apoptosis [J].J Thorac Cardiovasc Surg,1998,115(6):1310-1315.
    [38] Matsumoto T ,Tamaki T ,Kawakami M ,et al. Early complications of high2dose methylprednisolone sodium succinate treatment in the follow-up of acute cervical spinal cord injury [J].Spine,2001,26(4):426-430.
    [39] VAZIR IN D, LEE Y S, L IN C Y, et al. NAD ( P)H oxidase, superoxide dismutase, catalase, glutathione peroxidase and nitric oxide synthase exp ression in subacute sp inal cord injury [J].Brain Res,2004,995 (1) : 76-83
    [40] HALL E D. Pharmacological treatment of acute spinal cord injury: how do we build on past success [J].Sp inal CordMed,2001,24(3):142-146
    [41] EDWARD D, HALL, JOE E, et al. Neurop rotection and acute sp inal cord injury[J].A Reapp raisalNeurorx,2004,1(1):80-100
    [42] L IU J IN B O, TANG TIAN S I, YANG HU IL IN, et al. Antioxidation ofmelatonin against sp inal cord injury in rats[J].ChinMed J,2004,117(4):571-575
    [43] LEE Y S, SINDHU R K, L IN C Y, et al. Effects of nerve graft on nitric oxide synthase, NAD ( P) H oxidase, and antioxidant enzymes in chronic sp inal cord injury [J]. Free Radic BiolMed, 2004,36(3):330-339
    [44] 杨洁,高飞,易静.活性氧与细胞凋亡的研究进展[J].国外医学肿瘤学分册,2002,29(4):248-251
    [45] LUO J, SH I R. Acrolein induces axolemmal disruption, oxidative stress, and mitochondrial impairment in spinal cord tissue[J]. Neurochem Int,2004,44(7):475-486
    [46] ENOKIDO Y, HATANAKA H. Apop totic cell death occurs in hippocampal neurons cultured in a high oxygen atmosphere[J]. Neuroscience,1993,57:965-972
    [47] VAQUERO J, ZUR ITA M, OYA S, et al. Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced sp inal cord injury in rabbits [J].Spinal Cord,2002,40(5):224-229
    [48] KAMATA H, H IRATA H. Redox regulation of cellular signaling[J]. Cell Signal,1999 11(1):1–14
    [49] 谢萍.自由基与细胞凋亡[J].生物学教学,2004,1(29):3–4
    [50] Ng I, Yeo TT ,Tang WY,et al. Apoptosis occurs after cerebral contusions in humans[J].Neurosurgery,2000,46(4):949-956.
    [51] 刘一凡,石学敏.针灸抗氧化临床及实验研究进展.中国针灸1999,(2):124-127
    [52] 李威,范军铭,贾士奇等.电针对大鼠全脑缺血再灌注损伤的保护作用.中国针灸 1996,(11):21-22
    [1] 肖年来,姚共和.急性脊髓损伤模型的建立.中国中医骨伤科杂志,1999,7(6):49-51.
    [2] Vanicky I, Urdzikova L, Saganova K, et al. A simple and reproducible model of spinal cord injury induced by epidural balloon inflation in the rat.J Neurotrauma,2001,18(12):1399-1407.
    [3] Sheng H, Wang H, Homi HM, et al. A no-lam inectomy spinal cordcompression injury model in mice .J Neurotrauma,2004,21(5):595-603.
    [4] 杨迎暴,朴英杰.脊髓损伤模型的建立及其评价标准.中华创伤杂志,2002,18(3):187-190.
    [5] Metz GA, Curt A, vande Meent H, et al. Validation of the weight- drop contusion model in rats:a comparative study of human spinal cord injury. J Neurotrauma, 2000, 17(1):1-17.
    [6] Khan T, Havey RM ,Sayers ST,et al .Animal models of spinal cord contusion injuries.Lab Anim Sci,1999,49:161-172.
    [7] Thomas AJ, Nockels RP, Pan HQ, etal. Progesterone is neuroprotective after acute experimental spinal cord trauma in rats. Spine,1999,24:2134-2138.
    [8] 于如同,王其平,吴德模.电控大鼠脊髓损伤打击器的研制.中华创伤杂志,2005,21 (5):358-360.
    [9] 胥少汀,郭世绂.脊髓损伤基础与临床(第二版).北京:人民卫生出版社,2002,192-194.
    [10] Yeo SJ, Huang SN, Opark SW,et al.Development of rat model of grade contusive spinal cord injury using a pneumatic impact device. J Korean Sci,2004,19(4):574-580.
    [11] 陆宸熙,过邦辅,汤华丰.脊髓腹侧损伤实验模型.上海第二医学院学报,1983,1:15-17.
    [12] 谭炜,吴汝舟.实验性兔脊髓损伤打击器的改良和应用.大连医科大学学报,1998,20(4): 63-65.
    [13] 章慧平,陈忠,叶章群,等.多节段脊髓平面损伤后大鼠神经源性膀胱模型的制备. 临床外科杂志2007,15(3):196-197
    [14] 路华,冯忠堂,王廷华,等.挤压性脊髓损伤模型的制备.昆明医学院学报,2000,21(1):57-59.
    [15] Borgens RB.Cellular Engineering: molecular repair of membranes to rescue cells of the damaged nervous system.Neurosurgery, 2001, 49 (2):370-379.
    [16] Joshi M, Fehlings MG. Development and characterization of anovel, graded model of clip compressive spinal cord injury in the mouse: Part1. Clip design, behavioral out comes, and histopathology.J Neurotrauma,2002, 19(2):175-190.
    [17] Takahashi N, Yabuki S, Aoki Y ,et al. Pathomechanisms of nerve root injury caused by disc hemiation:an experimental study of mechanical compression and chemical imitation n.Spine,2003,28(5):435-441.
    [18] 张秋林,赵定麟,邱广义,等.大鼠脊髓腹侧压迫损伤模型的制备.第二军医大学学报,2000,21(4):396-397.
    [19] 张峡,王正国,朱佩芳.脊髓腹侧压迫损伤模型的建立与病理学观察.创伤外科杂志, 2004,6(3):164-166.
    [20] 宁斌,郑修军,胡有谷.慢性压迫性脊髓损伤动物模型的制作方法.中国脊柱脊髓杂志,2005,15(5): 316-318.
    [21] 孔抗美,齐伟力,周强,等.慢性渐进分级压迫大鼠脊髓损伤动物模型的研制.中医正骨,2005,17( 11):14-15.
    [22] Yamaguchi K, Murakami M, Takahashi K, et al..Behavioral and morphologic studies of the chronically compressed cauda equine: Experimental model of lumbar spinal stenosis in the rat.Spine,1999,24(9):845-851.
    [23] Pinazo, Seron MJ,Benet A,et al. Compression medular pormetastasis departs dehepatocar- cinoma. An Med Interna 1999,16(1):587-589
    [24] 伍亚民,廖维宏,王正国.脊髓损伤实验模型的研究概况与应用.中国临床康复,2003,7 (16):2344-2345.
    [25] 管玉龙,刘锋,董培青.脊髓缺血损伤动物模型的建立.中国体外循环杂志,2006,4(1):46-48.
    [26] 徐明,杨惠林,倪才方,等.经椎间动脉栓塞法建立急性脊髓缺血损伤模型.中华创伤杂志,2000,16(2):88-90.
    [27] 梁日生,周良辅,张荣,等.脊髓半切动物模型的制作及 SEP 和 MEP 监测.中国临床神经科学,2005,13(1):79-82.
    [28] 查韦光,郭晓明,王星星.实验性恒河猴脊髓半切损伤模型的建立.中华神经外科杂志,2006,22(5):309-311.
    [29] Talac R, Friedman J.A, Moore MJ, et al. Animal models of spinal cord injury for evaluation of tissue engineering treatment strategies.Biomaterials,2004,25(9):1505-1510.
    [30] 杨建华,陈杰,李长德.大鼠脊髓全横断模型的研究及其评价.黑龙江医药科学, 2006,29 (1):1-3.
    [31] 刘锐,游思维,刘惠玲,等.大鼠脊髓全横断损伤模型的建立.神经解剖学杂志, 2005,21(3):263-268.
    [32] 陈长青,李家顺,贾连顺,等.脊髓火器伤动物模型的建立.中国骨与关节损伤杂志,2005, 20(9)611-613.
    [33] 刘雷,裴福兴,杨效宁,等.大鼠牵张性脊髓损伤动物模型的建立和评价.创伤外科杂志,2005,7(2):106-109.
    [34] 罗伟,赵匡彦,王廷华.大鼠脊髓全横断模型制作及护理措施.昆明医学院学报,2004,(1):123-123.
    [1] Beattie MS, Farooqui AA, Bresnahan JC. Review of current evidence for apoptosis after spinal cord injury.J Neurotrauma,2000, 17(10):915-925
    [2] 徐水凌,顾旭东,顾敏.电穴刺激对脊髓损伤患者日常生活活动能力影响的研究.浙江中医杂志,2004,39(1):30-31.
    [3] 吴永刚,韩晶,孟维滨.针刺对大鼠脊髓损伤早期治疗作用的研究.上海针灸杂志,1995, 14 (4):182-183.
    [4] 吴永刚,刘成德,孙忠人,等.针刺对实验性脊髓损伤组织形态学的影响.上海针灸杂志, 1999,18(3):33-34.
    [5] 郑望苟,潘卫红,陈家禄。脊髓损伤后脊髓内丙二醛含量变化及其与神经功能损害的关系。中国康复医学杂志.2004,19(2):103~104
    [6] KontosHA,WeiIJP.Superoxidepro-ductioninexperimentalbraininjury.JNeurosurn,1989,64:803~809
    [7] HallED.InliibiliunoflipidperuxidaliuninCNSTrauma[J].Neurulrauma,1991,8:31~40.
    [8] 陈彦婷,陈宝友,冯凯琳,等.3MCP- 1 在中枢神经系统疾病中的表达及意义.武警医学院学报,2002;11(4):290~292
    [9] Frigeri A,Gropper MA,Umenishi F,et al,Localization of MIWC and GLIP water channel homologuesinneuromuscular,epithelialandglandular tissues[J].Cell Sci,1995,108:2993-3002.
    [10] SimpsonRK,JrRobertsonSD,GoodmanJC.Spinalcordischemiainducedelevationofaminoacids:extracellularmeasurementwithmicrodialysis[J].NeurochemRes,1990,15960:635~639
    [11] Fehlings MG,Tator CH.The effect of direct-current field on recovery from experimental spinal cord injury[J].Neurosurg,1988,68:781-792.
    [12] Yashon D.Edema of the spinal cord following experimental impact trauma
    [13] [J].Neur surg,1973,38:693.
    [14] HallED , BraughlerJM.Role of lipid peroxidation in post raumatic spinalcord degeneration-Areview.CNSTrauma,1986,3:281
    [15] Jike Lu,Ken i1S Ashwell,Phil Waite. Advances in secondary spinal cord injury:Role of apoptosis. Spine, 2000, 14:1859-1866
    [16] Satake K, Matsuyama Y, Kamiya M, et al .Nitric oxide via macrophage Inos induces apoptosis following traumatic spinal cord injury. Brain Res Mol Brain Res,2000,28:114-122
    [17] Esch F, Lin KI,Hills A, et al. Purification of a multipotent antideath activity from bovine liver and its identification as arginase: nitric oxide-independent nhibition of neuronal apoptosis. J Neurosci,1998,18:4083-4095
    [18] Kinoshita H. Pathology of spinal cord injuries due to fracture dislocation of the thoracic and lumbar spine. Paraplegia,1996,34:127.

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