安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
7期
883-886
,共4页
程岑%顾尔伟%鲁显福%刘训芹%张雷%陈菁菁
程岑%顧爾偉%魯顯福%劉訓芹%張雷%陳菁菁
정잠%고이위%로현복%류훈근%장뢰%진정정
舒芬太尼%后处理%脑缺血再灌注损伤
舒芬太尼%後處理%腦缺血再灌註損傷
서분태니%후처리%뇌결혈재관주손상
sufentanil%postconditioning%cerebral ischemia-reperfusion
目的:观察舒芬太尼后处理对大鼠大脑中动脉栓塞( MCAO)所致局灶性脑缺血再灌注损伤( CIRI )的保护作用。方法健康成年雄性SD大鼠70只,随机分为5组:假手术组(sham组),缺血再灌注组(IR组),舒芬太尼0.3μg/kg组( SP1组),舒芬太尼1μg/kg组( SP2组),舒芬太尼3μg/kg组( SP3组)。 IR组、SP1组、SP2组和SP3组动物均用线栓法制备右侧 MCAO模型,栓塞90 min 后恢复再灌注。SP1组、SP2组和SP3组于再灌注前5 min尾静脉注射舒芬太尼0.3、1、3μg/kg,sham组和IR组于再灌注前5 min尾静脉注射等容积生理盐水,均于1 min内注射完毕。于再灌注24 h行神经功能障碍( NDS)评分,随后每组取6只动物断头取脑行2,3,5-氯化三苯基四氮唑(TTC)染色,扫描并计算脑梗死容积百分比,每组剩余大鼠采用原位末端标记( TUNEL)法检测再灌注24 h皮层区缺血半暗带细胞凋亡。结果 IR后动物均表现一定程度神经功能障碍,再灌注24 h,SP2组及SP3组NDS评分明显低于IR组,脑梗死容积百分比明显低于IR组,皮层区缺血半暗带细胞凋亡指数明显低于IR组(P<0.05),而SP1组NDS评分、梗死容积百分比和凋亡指数与IR组间差异无统计学意义( P>0.05)。结论舒芬太尼1μg/kg后处理可减轻大鼠CIRI。
目的:觀察舒芬太尼後處理對大鼠大腦中動脈栓塞( MCAO)所緻跼竈性腦缺血再灌註損傷( CIRI )的保護作用。方法健康成年雄性SD大鼠70隻,隨機分為5組:假手術組(sham組),缺血再灌註組(IR組),舒芬太尼0.3μg/kg組( SP1組),舒芬太尼1μg/kg組( SP2組),舒芬太尼3μg/kg組( SP3組)。 IR組、SP1組、SP2組和SP3組動物均用線栓法製備右側 MCAO模型,栓塞90 min 後恢複再灌註。SP1組、SP2組和SP3組于再灌註前5 min尾靜脈註射舒芬太尼0.3、1、3μg/kg,sham組和IR組于再灌註前5 min尾靜脈註射等容積生理鹽水,均于1 min內註射完畢。于再灌註24 h行神經功能障礙( NDS)評分,隨後每組取6隻動物斷頭取腦行2,3,5-氯化三苯基四氮唑(TTC)染色,掃描併計算腦梗死容積百分比,每組剩餘大鼠採用原位末耑標記( TUNEL)法檢測再灌註24 h皮層區缺血半暗帶細胞凋亡。結果 IR後動物均錶現一定程度神經功能障礙,再灌註24 h,SP2組及SP3組NDS評分明顯低于IR組,腦梗死容積百分比明顯低于IR組,皮層區缺血半暗帶細胞凋亡指數明顯低于IR組(P<0.05),而SP1組NDS評分、梗死容積百分比和凋亡指數與IR組間差異無統計學意義( P>0.05)。結論舒芬太尼1μg/kg後處理可減輕大鼠CIRI。
목적:관찰서분태니후처리대대서대뇌중동맥전새( MCAO)소치국조성뇌결혈재관주손상( CIRI )적보호작용。방법건강성년웅성SD대서70지,수궤분위5조:가수술조(sham조),결혈재관주조(IR조),서분태니0.3μg/kg조( SP1조),서분태니1μg/kg조( SP2조),서분태니3μg/kg조( SP3조)。 IR조、SP1조、SP2조화SP3조동물균용선전법제비우측 MCAO모형,전새90 min 후회복재관주。SP1조、SP2조화SP3조우재관주전5 min미정맥주사서분태니0.3、1、3μg/kg,sham조화IR조우재관주전5 min미정맥주사등용적생리염수,균우1 min내주사완필。우재관주24 h행신경공능장애( NDS)평분,수후매조취6지동물단두취뇌행2,3,5-록화삼분기사담서(TTC)염색,소묘병계산뇌경사용적백분비,매조잉여대서채용원위말단표기( TUNEL)법검측재관주24 h피층구결혈반암대세포조망。결과 IR후동물균표현일정정도신경공능장애,재관주24 h,SP2조급SP3조NDS평분명현저우IR조,뇌경사용적백분비명현저우IR조,피층구결혈반암대세포조망지수명현저우IR조(P<0.05),이SP1조NDS평분、경사용적백분비화조망지수여IR조간차이무통계학의의( P>0.05)。결론서분태니1μg/kg후처리가감경대서CIRI。
Objective To investigate whether sufentanil postconditioning induces protection aganist focal cerebral ischemia-reperfusion injury in rats. Methods Seventy healthy adult male SD rats weighing 250~300 g were ran-domly divided into five groups. All rats in IR group,SP1 group,SP2 group and SP3 group were subjected to the right middle cerebral artery occlusion( MCAO) for 90 min and 24 h reperfusion. At 5 min before reperfusion, the rats were intravenously injected sufentanil 0. 3 μg/kg(SP1 group),1 μg/kg (SP2 group), 3 μg/kg (SP3 group) or normal saline ( sham group and IR group ) . The neurological deficit scores ( NDS ) were evaluated at 24 h after reperfusion,then all the animals were executed. Six rats in each group were executed to evaluate the infarct volume of the brain. The remaining rats in each group were executed to detect the apoptosis index. Infarct volume,as a percentage of volume at normal cerebral hemisphere,was determined by 2,3,5-triph-enyltetrazolium ( TTC) stai-ning. The neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay( TUNEL) . Results At 24 h after reperfusion,the neurological deficit scores and the apoptosis index in the SP2 group and SP3 group were significantly lower than those in the IR group(P<0. 05),the infarct volume in the SP2 group and SP3 group was significantly smaller than that in the IR group(P<0. 05). There were no sig-nificant differences in the neurological deficit scores,apoptosis index and infarct volume between groups of SP1 and IR. Conclusion Sufentanil postconditioning at a dosage of 1 μg/kg can provide neuroprotection against focal is-chemia-reperfusion injury in rats.