高压氧对大鼠脑缺血再灌注损伤后一氧化氮合酶阳性细胞分布和形态的影响
고압양대대서뇌결혈재관주손상후일양화담합매양성세포분포화형태적영향
Hyperbaric oxygen for nitric oxide synthase-positive neurons of rats following cerebral ischemia/reperfusion injury
  • 万方数据
    中国组织工程研究与临床康复 중국조직공정연구여림상강복
    JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
    2007年 25期 5050-5053 ,共4页

    曹义战%晋兴%查清%王伯良%仲月霞%付国强%何保健

    조의전%진흥%사청%왕백량%중월하%부국강%하보건

    脑缺血%一氧化氮合成酶%一氧化氮%神经元%大鼠 腦缺血%一氧化氮閤成酶%一氧化氮%神經元%大鼠
    뇌결혈%일양화담합성매%일양화담%신경원%대서
    背景:一氧化氮在脑缺血损伤中起着很重要的作用,而高压氧能改善缺血再灌注引起的神经损伤,高压氧的这种作用与一氧化氮是否有关联?其机制有待探讨.目的:观察一氧化氮合酶阳性细胞在大鼠急性局灶性脑缺血再灌注损伤和高压氧治疗后表达的变化.设计:随机对照动物实验.单位:解放军第四军医大学唐都医院急诊科;西安高新医院检验中心;解放军空军总医院.材料:取健康SD雄性大鼠66只,随机分为5组:假手术组5只,假手术+高压氧组5只,模型组28只,模型+高压氧组28只,后2组又分缺血后5,12,24,72 h 4个时间点,每个时间点7只.方法:①造模:模型组和模型+高压氧组大鼠参照Koizum方法制备大脑中动脉缺血模型,并于插入栓子造成缺血1 h后抽出栓子.其他2组手术,但不插入栓子.②高压氧治疗:假手术+高压氧组和模型+高压氧组大鼠分别在缺血后2,9,21,45,69 h共5次将动物置于高压氧舱内,给予高压氧(0.25 MPa绝对压)治疗1 h.主要观察指标:各组于相应时问点处死取脑,黄递酶-NADPH组织化学方法观察一氧化氮合酶阳性细胞在视交叉平面梗死区皮质、视前区、纹状体外侧区和纹状体内侧区域分布及形态的变化.结果:经补充后66只大鼠进入结果分析.①缺血后一氧化氮合酶阳性细胞发生形态改变,主要变化为突起减少或消失,细胞由椭圆形、三角形变成圆形,细胞皱缩,胞体着色重,胞核和胞浆均染成深蓝色;形态改变的一氧化氮合酶阳性细胞在纹状体外侧区最多,其次是视前区和纹状体内侧区,而皮质区较少.假手术组和假手术+高压氧组未见有形态改变的一氧化氮合酶阳性细胞.②模型组脑内形态有改变的一氧化氮合酶阳性细胞表达随缺血再灌注时间延长而增多,模型+高压氧组各时间点在皮质、视前区和纹状体内侧区其表达均比模型组少,但都于缺血后72 h至高峰[皮质:(15.46±3.02),(30.52±4173)个,视野;视前区:(28.56±4.05),(68.81±7.84)个/视野;纹状体内侧区:(21.09±3.83),(45.71±5.24)个/视野;P均＜0.01].结论:高压氧可明显抑制大鼠急性局灶性脑缺血再灌注损伤区一氧化氮合酶阳性细胞的变性,部位主要在皮质、视前区和纹状体内侧区.
    배경:일양화담재뇌결혈손상중기착흔중요적작용,이고압양능개선결혈재관주인기적신경손상,고압양적저충작용여일양화담시부유관련?기궤제유대탐토.목적:관찰일양화담합매양성세포재대서급성국조성뇌결혈재관주손상화고압양치료후표체적변화.설계:수궤대조동물실험.단위:해방군제사군의대학당도의원급진과;서안고신의원검험중심;해방군공군총의원.재료:취건강SD웅성대서66지,수궤분위5조:가수술조5지,가수술+고압양조5지,모형조28지,모형+고압양조28지,후2조우분결혈후5,12,24,72 h 4개시간점,매개시간점7지.방법:①조모:모형조화모형+고압양조대서삼조Koizum방법제비대뇌중동맥결혈모형,병우삽입전자조성결혈1 h후추출전자.기타2조수술,단불삽입전자.②고압양치료:가수술+고압양조화모형+고압양조대서분별재결혈후2,9,21,45,69 h공5차장동물치우고압양창내,급여고압양(0.25 MPa절대압)치료1 h.주요관찰지표:각조우상응시문점처사취뇌,황체매-NADPH조직화학방법관찰일양화담합매양성세포재시교차평면경사구피질、시전구、문상체외측구화문상체내측구역분포급형태적변화.결과:경보충후66지대서진입결과분석.①결혈후일양화담합매양성세포발생형태개변,주요변화위돌기감소혹소실,세포유타원형、삼각형변성원형,세포추축,포체착색중,포핵화포장균염성심람색;형태개변적일양화담합매양성세포재문상체외측구최다,기차시시전구화문상체내측구,이피질구교소.가수술조화가수술+고압양조미견유형태개변적일양화담합매양성세포.②모형조뇌내형태유개변적일양화담합매양성세포표체수결혈재관주시간연장이증다,모형+고압양조각시간점재피질、시전구화문상체내측구기표체균비모형조소,단도우결혈후72 h지고봉[피질:(15.46±3.02),(30.52±4173)개,시야;시전구:(28.56±4.05),(68.81±7.84)개/시야;문상체내측구:(21.09±3.83),(45.71±5.24)개/시야;P균＜0.01].결론:고압양가명현억제대서급성국조성뇌결혈재관주손상구일양화담합매양성세포적변성,부위주요재피질、시전구화문상체내측구.
    BACKGROUND: Nitric oxide (NO) plays an important role in the ischemic brain injury, and hyperbaric oxygen (HBO) can improve ischemia/reperfusion (I/R)-caused nerve injury. Whether the effect of HBO is associated with NO? Its mechanism needs to be further investigated.OBJECTIVE: To observe the changes of expression of nitric oxide synthase (NOS)-positive neurons of rats following acute focal cerebral I/R injury and HBO treatment.DESIGN: Randomized controlled animal experiment.SETTING: Department of Emergency, Tangdu Hospital, Fourth Military Medical University of Chinese PLA; Department of Laboratory Medicine, Xi'an Gaoxin Hospital; The General Hospital of the Air Force of Chinese PLA.MATERIALS : Sixty-six healthy male Sprague-Dawley rats were chosen and randomized into 5 groups: sham-operation group (n =5), sham-operation +HBO treatment group (n =5), model group (n =28), modeling +HBO treatment group (n =28). Ischemia 5,12, 24 and 72 hours four time points were set in the later 2 groups, 7 rats at each time point.METHODS: ①Rats in the model group and modeling+ HBO treatment group were created into models of middle cerebral artery ischemia according to the method from Koizum. Then, an embolus was inserted for ischemia; One hour later, the embolus was drawn out. Inserting embolus was omitted in the other two groups.②Rats in the sham operation + HBO treatment group and modeling + HBO treatment group were placed in HBO chamber at ischemia 2, 9, 21, 45 and 69 hours, separately, and given HBO treatment for 1 hour (0.25 MPa absolute pressure).MAIN OUTCOME MEASURES: The rats in each group were sacrificed at corresponding time points, and their brains were harvested. The distribution and morphology of NOS positive cells in cortical area, preoptic area, lateral and medial corpora striata of infarct region at the level of optic chiasma were observed with nicotinamide-adenine dinucleotide phosphate -diaphorase (NADPH-d) histochemical method.RESULTS: After supplement, 66 rats were involved in the final analysis. ①After ischemia, NOS-positive neurons changed in morphology, mainly presenting prominences were reduced or disappeared, neurons changed from ellipse or triangle into global shape, and shrank; Body of neuron darkly dyed; Both nucleus and cytoplasm were deeply dyed into dark blue; NOS-positive neurons with changed morphology were mostly in lateral corpora striatum, followed by preoptic area and medial corpora striatum, and those in the cortical area were few. NOS-positive neurons with changed morphology were not found in the sham-operation group and sham-operation + HBO treatment group. ②In the model group, NOS-positive neurons with changed morphology were increased with elongation of I/R time. At each time point, NOS-positive neurons in cortical area, preoptic area and medial corpora striatum in modeling + HBO treatment group were less than those in model group, but NOS-positive neurons in two groups both reached their peaks at ischemia 72 hours [Cortical area: (15.46±3.02) vs.(30.52±4.73)/visual field; Preoptic area:(28.56±4.05) vs. (68.81±7.84)/visual field; medial corpora striatum:(21.09±3.83) vs.(45.71±5.24)/visual field; all P＜0.01].CONCLUSION: HBO obviously inhibits the degeneration of NOS-positive neurons in acute focal cerebral I/R injury regions of rats, such as cortical area, preoptic area, medial corpora striatum, and so on
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