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蛛网膜下腔出血后海马区微血管痉挛及血管内转染一氧化氮合酶基因的影响
引用本文:张珑,钱锁开,黄国兵,等. 蛛网膜下腔出血后海马区微血管痉挛及血管内转染一氧化氮合酶基因的影响[J]. 中华老年心脑血管病杂志, 2014, 0(4): 425-427
作者姓名:张珑  钱锁开  黄国兵  
作者单位:解放军第九四医院神经外科;宜春市人民医院神经外科;
摘    要:目的研究蛛网膜下腔出血(SAH)后海马CA1区神经元及微血管的变化,观察血管内转染内皮型一氧化氮合酶(eNOS)基因后,海马CA1神经元及微血管改变,探讨eNOS基因转染预防脑血管痉挛的作用。方法 24只兔随机分为对照组、SAH组、转染携带eNOS基因重组腺病毒组(AdeNOS组)。每组8只。采用枕大池二次注血法制备兔SAH后脑血管痉挛模型。兔于首次注血后7d进行灌注固定,留取海马区脑组织标本,在电镜和光镜下观察海马神经元及微血管的变化。结果光镜下SAH组海马CA1区神经元较对照组明显减少,微血管周围间隙增宽,管腔狭窄,管壁增厚;电镜下SAH组海马神经元细胞肿胀,结构不完整,细胞核固缩,线粒体空泡化;AdeNOS组损伤较SAH组明显减轻。结论 SAH后脑血管痉挛可引起海马CA1区神经元变性,可能与海马区微血管痉挛改变有关,eNOS基因转染可明显减轻海马神经元损伤,预防SAH后脑血管痉挛的发生。

关 键 词:蛛网膜下腔出血  海马  一氧化氮合酶  转染  血管痉挛,颅内

Effect of subarachnoid cavity hemorrhage on hippocampus microvascular spasm and intravascular nitric oxide synthase gene transfection
Abstract:Objective To sdudy the effect of subarachnoid cavity hemorrhage(SAH)on hippocampus microvascular spasm and intravascular nitric oxide synthase gene transfection.MethodsTwenty-four rabbits were randomly divided into control group,SAH group,and AdeNOS group(8in each group).A cerebrovascular spasm model was established by injecting blood into the occipital pool.Hippocampus tissue samples were fixed by perfusion.Neurons in hippocampal CA1 region and microvascular spasm were observed under optical microscope.Results Optical microscopy showed that the number of neurons in hippocampal CA1region was significantly less,the microvascular perivascular space was significantly wider,the vascular stenosis was severer,and the vascular wall was significantlt thicker in SAH group than in control group.Electron microscopy displayed that the neurons in hippocampal CA1region were swollen,with intact structures, condensed nuclei,and vacuoled mitochondria in SAH group.The injury was significantly milder in AdeNOS group than in SAH group.Conclusion Cerebrovascular spasm following SAH can lead to degeneration of neurons in hippocampal CA1region,which may be related with the hippocampus microvascular spasm.Transfection of endothelial nitric oxide synthase gene can markedly alleviate the injury of hippocampal neurons and prevent cerebral vascular spasm following SAH.
Keywords:subarachnoid hemorrhage  hippocampus  nitric oxide synthase  transfection  vasospasm,intracranial
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