中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
10期
1242-1244
,共3页
异氟醚%脂肪乳剂,静脉注射用%膜蛋白质类%再灌注损伤%脑%缺血预处理
異氟醚%脂肪乳劑,靜脈註射用%膜蛋白質類%再灌註損傷%腦%缺血預處理
이불미%지방유제,정맥주사용%막단백질류%재관주손상%뇌%결혈예처리
Isoflurane%Fat emulsions,intravenous%Membrane proteins%Reperfusion injury%Brain%Ischemic preconditioning
目的 探讨乳化异氟醚预处理对大鼠局灶性脑缺血再灌注时脑组织突触后致密物质95(PSD95)活化的影响.方法 雄性清洁级SD大鼠32只,体重280 ～ 300 g,采用随机数字表法,将大鼠随机分为4组(n=8):假手术组(S组)、缺血再灌注组(I/R组)、乳化异氟醚组(EI组)和脂肪乳剂组(LE组).采用大脑中动脉阻塞法制备局灶性脑缺血再灌注模型.EI组和LE组分别腹腔注射8％乳化异氟醚10.5 ml/mg或30％脂肪乳10.5 ml/mg,24h后制备模型.再灌注6h时行神经功能缺陷评分,随机取4只大鼠,处死后取缺血侧海马和皮层组织,采用Western blot法检测磷酸化的PSD95( pPSD95)的表达水平.再灌注24 h时,随机取4只大鼠,处死后取脑组织,计算脑梗死体积百分比.结果 S组未见神经功能缺陷和脑梗死发生.与S组比较,I/R组、EI组和LE组神经功能缺陷评分、脑梗死体积百分比、海马和皮质pPSD95表达水平升高(P＜0.01)；与I/R组比较,EI组神经功能缺陷评分、脑梗死体积百分比、海马和皮质pPSD95表达水平降低(P＜0.05),LE组差异无统计学意义(P＞0.05).结论乳化异氟醚可通过抑制脑组织PSD95的活化,减轻大鼠局灶性脑缺血再灌注损伤.
目的 探討乳化異氟醚預處理對大鼠跼竈性腦缺血再灌註時腦組織突觸後緻密物質95(PSD95)活化的影響.方法 雄性清潔級SD大鼠32隻,體重280 ～ 300 g,採用隨機數字錶法,將大鼠隨機分為4組(n=8):假手術組(S組)、缺血再灌註組(I/R組)、乳化異氟醚組(EI組)和脂肪乳劑組(LE組).採用大腦中動脈阻塞法製備跼竈性腦缺血再灌註模型.EI組和LE組分彆腹腔註射8％乳化異氟醚10.5 ml/mg或30％脂肪乳10.5 ml/mg,24h後製備模型.再灌註6h時行神經功能缺陷評分,隨機取4隻大鼠,處死後取缺血側海馬和皮層組織,採用Western blot法檢測燐痠化的PSD95( pPSD95)的錶達水平.再灌註24 h時,隨機取4隻大鼠,處死後取腦組織,計算腦梗死體積百分比.結果 S組未見神經功能缺陷和腦梗死髮生.與S組比較,I/R組、EI組和LE組神經功能缺陷評分、腦梗死體積百分比、海馬和皮質pPSD95錶達水平升高(P＜0.01)；與I/R組比較,EI組神經功能缺陷評分、腦梗死體積百分比、海馬和皮質pPSD95錶達水平降低(P＜0.05),LE組差異無統計學意義(P＞0.05).結論乳化異氟醚可通過抑製腦組織PSD95的活化,減輕大鼠跼竈性腦缺血再灌註損傷.
목적 탐토유화이불미예처리대대서국조성뇌결혈재관주시뇌조직돌촉후치밀물질95(PSD95)활화적영향.방법 웅성청길급SD대서32지,체중280 ～ 300 g,채용수궤수자표법,장대서수궤분위4조(n=8):가수술조(S조)、결혈재관주조(I/R조)、유화이불미조(EI조)화지방유제조(LE조).채용대뇌중동맥조새법제비국조성뇌결혈재관주모형.EI조화LE조분별복강주사8％유화이불미10.5 ml/mg혹30％지방유10.5 ml/mg,24h후제비모형.재관주6h시행신경공능결함평분,수궤취4지대서,처사후취결혈측해마화피층조직,채용Western blot법검측린산화적PSD95( pPSD95)적표체수평.재관주24 h시,수궤취4지대서,처사후취뇌조직,계산뇌경사체적백분비.결과 S조미견신경공능결함화뇌경사발생.여S조비교,I/R조、EI조화LE조신경공능결함평분、뇌경사체적백분비、해마화피질pPSD95표체수평승고(P＜0.01)；여I/R조비교,EI조신경공능결함평분、뇌경사체적백분비、해마화피질pPSD95표체수평강저(P＜0.05),LE조차이무통계학의의(P＞0.05).결론유화이불미가통과억제뇌조직PSD95적활화,감경대서국조성뇌결혈재관주손상.
Objective To investigate the effect of emulsified isoflurane preconditioning on postsynaptic density protein 95 (PSD95) activation in brain during focal cerebral ischemia-reperfusion (I/R)injury in rats.Methods Thirty-two pathogen-free male SD rats weighing 280-300 g were randomly divided into 4 groups (n =8each): sham operation group(group S),group I/R,emulsified isoflurane group(group EI) and lipid emulsion group(group LE).Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 h followed by reperfusion.8％ emulsified isoflurane 10.5 ml/mg or 30％ lipid emulsion 10.5 ml/mg was injected intraperitoneally at 24h before I/R in groups EI and LE respectively.The neurologic deficit score (NDS) was evaluated at 6 h of reperfusion and then 4 rats were sacrificed,and brains were removed for determination of phosphorylatied PSD95 (pPSD95) expression in ischemia cortex and hippocampus by Western blot.Four rats were sacrificed at 24 h of reperfusion and then their brains were removed for determination of infarct volume percentage.Results NDS,infarct volume percentage and pPSD95 expression in ischemia cortex and hippocampus were higher in groups I/R,EI and LE than in group S( P ＜ 0.01 ).NDS,infarct volume percentage and pPSD95 expression in ischemia cortex and hippocampus were lower in group EI than in group I/R( P ＜ 0.05).There was no significant difference in NDS,infarct volume percentage and pPSD95 expression between groups I/R and LE(P ＞ 0.05).Conclusion Emulsified isoflurane preconditioning can attenuate focal cerebral I/R injury in rats by inhibiting PSD95 activation in brain.
