中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
6期
550-552
,共3页
刘旭冬%于灵芝%韩友群%姜丽
劉旭鼕%于靈芝%韓友群%薑麗
류욱동%우령지%한우군%강려
再灌注损伤%脑%内皮抑素类%血管内皮生长因子类
再灌註損傷%腦%內皮抑素類%血管內皮生長因子類
재관주손상%뇌%내피억소류%혈관내피생장인자류
Reperfusion injury%Brain%Endostatins%Vascular endothelial growth factors
目的 探讨大鼠脑缺血再灌注损伤时脑组织血管内皮生长因子(VEGF)和内皮抑素(ES)的变化.方法 雄性Wistac大鼠48只,体重270～330 g,随机分为2组:假手术组(S组,n=8)和脑缺血再灌注组(IR组,n=40).IR组采用改良的Zea Longa线栓法阻断大鼠左侧大脑中动脉建立局灶性脑缺血再灌注模型,缺血90 min时拔出线栓行再灌注.S组只插入线栓,不阻断大脑中动脉.S组于术后1 d时、IR组分别于再灌注6 h、1、2、4、7 d时,取8只大鼠进行神经功能损伤评分,然后处死,取脑组织,观察脑梗死情况,采用RT-PCR法测定VEGF mRNA和ES mRNA的表达,计算其比值(ES/VEGF).结果 与S组相比,IR组再灌注各时点神经功能损伤评分升高,脑组织VEGF mRNA表达上调,再灌注1、2、4、7 d时脑组织ES mRNA表达上调,再灌注2、4、7 d时脑组织ES/VEGF降低(P<0.01).再灌注2 d时神经功能损伤评分最高,VEGF mRNA表达及ES/VEGF至谷值,ES mRNA表达至峰值,脑梗死最严重.结论 大鼠脑缺血再灌注时VEGF mRNA和ES mRNA表达上调,且脑损伤程度与脑组织ES和VEGF的平衡状态有关.
目的 探討大鼠腦缺血再灌註損傷時腦組織血管內皮生長因子(VEGF)和內皮抑素(ES)的變化.方法 雄性Wistac大鼠48隻,體重270～330 g,隨機分為2組:假手術組(S組,n=8)和腦缺血再灌註組(IR組,n=40).IR組採用改良的Zea Longa線栓法阻斷大鼠左側大腦中動脈建立跼竈性腦缺血再灌註模型,缺血90 min時拔齣線栓行再灌註.S組隻插入線栓,不阻斷大腦中動脈.S組于術後1 d時、IR組分彆于再灌註6 h、1、2、4、7 d時,取8隻大鼠進行神經功能損傷評分,然後處死,取腦組織,觀察腦梗死情況,採用RT-PCR法測定VEGF mRNA和ES mRNA的錶達,計算其比值(ES/VEGF).結果 與S組相比,IR組再灌註各時點神經功能損傷評分升高,腦組織VEGF mRNA錶達上調,再灌註1、2、4、7 d時腦組織ES mRNA錶達上調,再灌註2、4、7 d時腦組織ES/VEGF降低(P<0.01).再灌註2 d時神經功能損傷評分最高,VEGF mRNA錶達及ES/VEGF至穀值,ES mRNA錶達至峰值,腦梗死最嚴重.結論 大鼠腦缺血再灌註時VEGF mRNA和ES mRNA錶達上調,且腦損傷程度與腦組織ES和VEGF的平衡狀態有關.
목적 탐토대서뇌결혈재관주손상시뇌조직혈관내피생장인자(VEGF)화내피억소(ES)적변화.방법 웅성Wistac대서48지,체중270～330 g,수궤분위2조:가수술조(S조,n=8)화뇌결혈재관주조(IR조,n=40).IR조채용개량적Zea Longa선전법조단대서좌측대뇌중동맥건립국조성뇌결혈재관주모형,결혈90 min시발출선전행재관주.S조지삽입선전,불조단대뇌중동맥.S조우술후1 d시、IR조분별우재관주6 h、1、2、4、7 d시,취8지대서진행신경공능손상평분,연후처사,취뇌조직,관찰뇌경사정황,채용RT-PCR법측정VEGF mRNA화ES mRNA적표체,계산기비치(ES/VEGF).결과 여S조상비,IR조재관주각시점신경공능손상평분승고,뇌조직VEGF mRNA표체상조,재관주1、2、4、7 d시뇌조직ES mRNA표체상조,재관주2、4、7 d시뇌조직ES/VEGF강저(P<0.01).재관주2 d시신경공능손상평분최고,VEGF mRNA표체급ES/VEGF지곡치,ES mRNA표체지봉치,뇌경사최엄중.결론 대서뇌결혈재관주시VEGF mRNA화ES mRNA표체상조,차뇌손상정도여뇌조직ES화VEGF적평형상태유관.
Objective To investigate the changes in vascular endothelial growth factor (VECF) and endostatin (ES) in rat brain tissues following cerebral ischemia-reperfusion (IR) injury. Methods Forty-eight male Wistar rats weighing 270-330 g were randomly divided into 2 groups: sham operation group (group S, n = 8) and IR group ( n = 40). The animals were anesthetized with intraperitoneal chloral hydrate 3 ml/kg. Left common, internal and external carotid arteries (CCA, ICA, ECA) were exposed. Middle cerebral artery occlusion (MCAO) was produced by inserting a nylon thread 17-19 mm in length into ICA and advancing it cranially until resistance was felt using Zea Longa's method. At 90 min of MCAO, the nylon thread was withdrawn to allow reperfusion. In group S, the nylon thread was inserted 10 mm in length into ICA but no MCAO was performed. The neurological deficit was scored at 1 d after operation in group S, and at 6h, 1 d, 2 d, 4 d and 7 d of reperfusion in group IR (8 animals at each time point) . The rats were then killed and the brains were removed and sliced. Brain tissue slices from 2 out of the 8 rats were stained with triphenyl tetrazolium chloride to estimate the infarct size, while those from the other 6 rats were used to determine the expression of VEGF mRNA and ES mRNA using RT-PCR. ES/VEGF ratio was calculated. Results Compared with group S, neurological deficit score was significantly increased and VEGF mRNA expression in brain tissues was up-regulated at each time point following reperfusion, ES mRNA expression in brain tissues was up-regulated at 1, 2, 4 and 7 d of reperfusion, and ES/VEGF ratio in brain tissues was significantly decreased at 2, 4 and 7 d of reperfusion in group IR ( P < 0.01). The neurological deficit score was the highest, expression of VEGF mRNA and ES/VEGF ratio reached the valley value ES mRNA, expression reached the peak value, and infarct size was the largest at 2 d of reperfusion. Conclusion The expression of VEGF mRNA and ES mRNA is up-regulated during cerebral IR in rats and the degree of brain injury may be related to the balance of ES and VEGF in brain tissues.
