摘要
目的:观察星状神经节阻滞对全脑缺血再灌注后家兔海马CA1区凋亡基因bax,bcl-2表达的影响,分析其对脑缺血再灌注损伤的效应及其作用。方法:实验于2004-08/2005-02在郧阳医学院附属太和医院神经疾病研究所进行。①21只雄性日本大耳白兔随机分成实验组、对照组、假手术组,每组7只。②无菌操作下暴露左侧星状神经节及双侧颈内、颈外动脉及椎动脉,在星状神经节旁埋置导管。实验组夹闭上述“六血管”缺血10min后松开动脉夹再恢复灌注24h,缺血前于星状神经节处推注2.5g/L布比卡因0.5mL后再用微量泵以0.5mL/h的速度注药行持续星状神经节阻滞,对照组也进行缺血再灌注,缺血前暴露星状神经节,假手术组仅分离血管和暴露星状神经节而不阻断血流。③各组动物于再灌注后24h行神经功能缺陷评分,随后灌注固定取脑组织,免疫组织化学染色检测海马CA1区Bax和Bcl-2的表达。结果:实验中有2只动物分别死于麻醉意外和神经反射所致的心跳骤停。死亡后随机补充,保证21只动物进入结果分析。①实验组、对照组、假手术组家兔海马CA1区Bax表达阳性细胞数分别为(23.1±1.9)个/视野、(39.7±2.8)个/视野、(13.3±1.7)个/视野,前两者与后者相比差异有显著性意义(P<0.01),而对照组的增加高于实验组,差异有显著性意义(P<0.05)。②实验组家兔海马CA1区Bcl-2表达明显高于假手术组(0.131±0.015),(0.094±0.008),(P<0.05),而对照组增加不明显(0.101±0.013),与假手术组比较差异无显著性意义(P>0.05)。③实验组动物神经功能缺陷评分(22.7±2.8)显著低于对照组(27.3±2.9,P<0.05)。结论:星状神经节阻滞可降低全脑缺血再灌注后家兔神经功能缺陷评分,促进海马CA1区Bcl-2的表达,抑制Bax的表达,提示其可能参与脑保护作用的机制。
AIM： To observe the effects of stellate ganglion block （SGB） expressions of apoptotic genes Bax and Bcl-2 in hippocampus CA1 of rabbits with cerebral ischemic repeffusion and analyze its effects on cerebral ischemic reperfusion injury.
METHODS： The experiment was conducted in the Department of Neural Disease, Affiliated Taihe Hospital of Yunyang Medical College from August 2004 to February 2005.（1）21 Japanese male rabbits were randomly divided into experimental group, control group and sham-operation group with 7 rabbits in each group.（2）Stellate ganglion （SG） in the left side, bilateral external and internal carotid arteries as well as vertebral arteries were exposed in sterile operation, tubes were embedded near the SG, ＂six vessles＂ mentioned above in rabbits of experimental group were clamped, 10 minutes after that, clamps were loosened for 24-hour reperfusion; Bupivacaine was injected at 0.5 mL per hour with micro pump to maintain stellate block following injection of 0.5 mL bupivacaine in SG before ischemia according to 2.5 g/L. Rabbits in control group received ischemic reperfusion whose SGs were exposed before ischemia; Vessels of rabbits in the sham-operation group were seperated and SGs were exposed without blood flow occluded. （3）Neurofunctional deficit scores of all rabbits were evaluated at 24 hours after reperfusion, rabbits were fixed with perfusion to take brain tissues out. Expressions of Bax and Bcl-2 in hippocampus CA1 were： detected with immunohistochemical stain.
RESULTS： Two rabbits died from anesthetic accident and cardiac arrest induced by nervous reflex respectively, another two rabbits were randomly selected to enable totally 21 animals be involved in the analysis of results, （1）Positive cell population in expressions of Box in hippocampus CA1 of rabbits in experimental group, controls group and sham-operation group were respectively （23.1±1.9）, （39.7±2.8） and （13.3±1.7） per visual field. Differences between first two group and the latter one were remarkable （P 〈 0.01）, while increasing in the control group was much higher than that in experimental group （P 〈 0.05）.（2）Expression of Bcl-2 in hippocampus CA1 of rabbits in experimental group was obviously higher than that in the sham-operation group （0.131 ±0.015）, （0.094±0.008）, （P 〈 0.05）, while increasing in the control group was not remarkable （0.101 ±0.013）, differences between control group and sham-operation group were not marked （P 〉 0.05）. （3）Neurofunctional deficit score of rabbits in the experimental group （22.7 ±2.8） was remarkably lower than that in the control group（27.3±2.9） （P 〈 0.05）.
CONCLUSION： SGB can decrease the neurofunctional deficit score, improve the expression of Bcl-2 in hippocampus CA1 and depress the expression of Bax in rabbits with total cerebral ischemic reperfusion, which indicates that it may be involved in the protective mechanism on brain.
出处
《中国临床康复》
CSCD
北大核心
2006年第14期105-107,共3页
Chinese Journal of Clinical Rehabilitation
基金
湖北省教育厅优秀中青年人才科研计划资助项目(2002B03001)~~
