中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
12期
1479-1481
,共3页
谢春林%胡宪文%孔令锁%吴运香%李光武%张野
謝春林%鬍憲文%孔令鎖%吳運香%李光武%張野
사춘림%호헌문%공령쇄%오운향%리광무%장야
哌啶类%再灌注损伤%脑%认知障碍
哌啶類%再灌註損傷%腦%認知障礙
고정류%재관주손상%뇌%인지장애
Piperidines%Reperfusion injury%Brain%Cognition disorders
目的 探讨瑞芬太尼后处理对脑缺血再灌注大鼠海马神经元凋亡的影响.方法 健康成年雄性SD大鼠24只,体重250~300 g,随机分为4组(n=6):假手术组(S组)、缺血再灌注组(IR组)、瑞芬太尼0.6μg·kg-1·min-1组(R1组)和瑞芬太尼1.8μg·kg-1·min-1组(R2组).采用夹闭双侧颈总动脉联合低血压法制备大鼠全脑缺血再灌注模型.R1组和R2组分别于再灌注前5 min泵注瑞芬太尼0.6、1.8μg·kg-1·min-1,注射时间5 min.于再灌注第3天采用Morris水迷宫实验及跳台实验测定大鼠认知功能.水迷宫实验结束后,处死大鼠取脑分离海马,采用免疫组化法检测海马CA1区caspase-3蛋白的表达,TUNEL法检测神经元凋亡情况.结果 与S组相比,IR组、R1组和R2组大鼠认知功能减退,海马CA1区神经元凋亡数目升高,IR组caspase-3表达上调(P<0.05);与IR组相比,R1组和R2组大鼠认知功能提高,海马CA1区caspase-3表达水平和凋亡神经元数目降低(P<0.05).结论 瑞芬太尼后处理可通过下调caspase-3表达,抑制海马神经元凋亡,从而改善脑缺血再灌注大鼠的认知功能.
目的 探討瑞芬太尼後處理對腦缺血再灌註大鼠海馬神經元凋亡的影響.方法 健康成年雄性SD大鼠24隻,體重250~300 g,隨機分為4組(n=6):假手術組(S組)、缺血再灌註組(IR組)、瑞芬太尼0.6μg·kg-1·min-1組(R1組)和瑞芬太尼1.8μg·kg-1·min-1組(R2組).採用夾閉雙側頸總動脈聯閤低血壓法製備大鼠全腦缺血再灌註模型.R1組和R2組分彆于再灌註前5 min泵註瑞芬太尼0.6、1.8μg·kg-1·min-1,註射時間5 min.于再灌註第3天採用Morris水迷宮實驗及跳檯實驗測定大鼠認知功能.水迷宮實驗結束後,處死大鼠取腦分離海馬,採用免疫組化法檢測海馬CA1區caspase-3蛋白的錶達,TUNEL法檢測神經元凋亡情況.結果 與S組相比,IR組、R1組和R2組大鼠認知功能減退,海馬CA1區神經元凋亡數目升高,IR組caspase-3錶達上調(P<0.05);與IR組相比,R1組和R2組大鼠認知功能提高,海馬CA1區caspase-3錶達水平和凋亡神經元數目降低(P<0.05).結論 瑞芬太尼後處理可通過下調caspase-3錶達,抑製海馬神經元凋亡,從而改善腦缺血再灌註大鼠的認知功能.
목적 탐토서분태니후처리대뇌결혈재관주대서해마신경원조망적영향.방법 건강성년웅성SD대서24지,체중250~300 g,수궤분위4조(n=6):가수술조(S조)、결혈재관주조(IR조)、서분태니0.6μg·kg-1·min-1조(R1조)화서분태니1.8μg·kg-1·min-1조(R2조).채용협폐쌍측경총동맥연합저혈압법제비대서전뇌결혈재관주모형.R1조화R2조분별우재관주전5 min빙주서분태니0.6、1.8μg·kg-1·min-1,주사시간5 min.우재관주제3천채용Morris수미궁실험급도태실험측정대서인지공능.수미궁실험결속후,처사대서취뇌분리해마,채용면역조화법검측해마CA1구caspase-3단백적표체,TUNEL법검측신경원조망정황.결과 여S조상비,IR조、R1조화R2조대서인지공능감퇴,해마CA1구신경원조망수목승고,IR조caspase-3표체상조(P<0.05);여IR조상비,R1조화R2조대서인지공능제고,해마CA1구caspase-3표체수평화조망신경원수목강저(P<0.05).결론 서분태니후처리가통과하조caspase-3표체,억제해마신경원조망,종이개선뇌결혈재관주대서적인지공능.
Objective To investigate the effects of remifentanil postconditioning on apoptosis in hippocampal neruons in a rat model of cerebral ischemia-reperfusion(I/R)and the mechanism involved.Methods Twentyfour male SD rats weighing 250-300 g were randomly divided into 4 groups(n = 6 each): sham operation group (group S);global cerebral I/R group(group I/R);remifentanil 0.6μg·kg- 1·min-1+global cerebral I/R group (group R1)and remifentanil 1.8μg·kg-1·min-1 + global cerebral I/R group(group R2).Global cerebral ischemia was induced by 10 min occlusion of bilateral common carotid combined with hypotension.In group R1 and R2,remifentanil at 0.6 and 1.8μg·kg-1·min-1 were infused for 5 min before ischemia respectively.The cognitive function was tested with Morris water maze and step-down tests from the day 3 to day 8 after reperfusion.When Morris water maze test was finished,rat brains were removed for HE staining and determination of the expression of caspase-3 in hippocampal CA1 region by immuno-histochemistry.Apoptosis in neurons in hippocampal CA1 region was detected by TUNEL assay.Results Compared with group S,the cognitive function was significantly decreased and the number of apopotic neurons in hippocampus CA1 region increased in group I/R,R1 and R2,and the expression of caspase-3 was up-regulated in group I/R(P<0.05).Compared with group I/R,the cognitive function was significantly increased,the expression of caspase-3 was down-regulated,and the number of apopotic neurons in hippocampus CA1 region was significantly decreased in group R1 and R2(P<0.05).Conclusion Remifentanil postconditioning can improve the cognitive function through down-regulating caspase-3 expression and inhibiting the apoptosis in hippocampal neruons in a rat model of cerebral I/R.