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机构地区:[1]中南大学湘雅医院神经外科,湖南长沙410007
出 处:《海南医学》2012年第9期27-31,共5页Hainan Medical Journal
摘 要:目的研究芬太尼(Fentanyl)对蛛网膜下腔出血后脑血管痉挛的影响及其作用机制。方法选用健康成年家兔72只,随机分成假手术对照组(A组)、SAH组(B组)、芬太尼静脉干预组(C组)、芬太尼肌注干预组(D组)。每天进行神经生物学评分,并在实验24h、72h、7d后处死,取基底动脉进行H-E染色,观察管壁情况,同时取左侧海马分别行HE染色及免疫组化染色,观测神经元密度、Bcl-2及Bax的表达。结果 SAH后Bcl-2、Bax表达均增加,芬太尼干预后Bcl-2表达升高,Bax表达下降。B组的神经生物学评分、神经元密度、Bcl-2及Bax的表达与C、D组差异有统计学意义(P<0.05)。结论芬太尼可抑制CVS后细胞凋亡,可能通过促进SAH家兔Bcl-2的表达而抑制Bax表达。Objective To study the effect of Fentanyl on cerebral vasospasm after subarachnoid hemorrhage and its mechanism.Methods Seventy-two healthy adult rabbits were randomly divided into four groups:the control group (group A),SAH group (group B),SAH with fentanyl intravenous (group C) and SAH with fentanyl intramuscular (group D).The rabbits underwent neurobiology score every day.The basar artery was stained by HE,and hippocampus undrewent HE staining and Bcl-2/Bax immunohistochemical staining,then the neuron density as well as the expression of Bax and Bcl-2 were detected.Results After SAH,the expression of Bcl-2 and Bax increased.After intervention with fentanyl,the expression Bcl-2 was increased,while the expression of Bax decreased.,The neurological function score,neuron density and Bax and Bcl-2 expression in group B showed statistically significant differences with those in group C and group D (P0.05).Conclusion Fentanyl can inhibit neuron apoptosis possibly through enhancing Bcl-2 expression and inhibiting Bax expression.
关 键 词:脑血管痉挛 芬太尼 家兔 脑保护 BAX BCL-2
分 类 号:R743[医药卫生—神经病学与精神病学]
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