中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
2期
221-224
,共4页
异氟醚%脂肪乳剂,静脉注射用%再灌注损伤%血小板活化因子%受体,细胞表面%脑
異氟醚%脂肪乳劑,靜脈註射用%再灌註損傷%血小闆活化因子%受體,細胞錶麵%腦
이불미%지방유제,정맥주사용%재관주손상%혈소판활화인자%수체,세포표면%뇌
Isoflurane%Fat emulsions,intravenous%Reperfusion injury%Platelet activating factor%Receptors,cell surface%Brajn
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血小板活化因子( PAF)及其受体表达的影响.方法 健康成年雄性SD大鼠32只,体重250～300 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)和脂肪乳组(LE组).采用线栓阻塞大脑中动脉2h行再灌注的方法制备大鼠局灶性脑缺血再灌注损伤模型.于缺血前24h,S组和I/R组腹腔注射生理盐水10.5 ml/kg,EI组和LE组分别给予8％乳化异氟醚和30％脂肪乳10.5 ml/kg.再灌注12 h时进行神经功能缺陷评分,随后每组处死4只大鼠,采用TTC染色法测定脑梗死体积,每组取其余4只大鼠,采集静脉血样,采用ELISA法测定血浆PAF浓度,随后处死大鼠,分离海马和皮层,采用Western blot法测定PAF受体的表达.结果 与S组比较,其余3组神经功能缺陷评分评分、脑梗死体积百分比、血浆PAF浓度、海马和皮层PAF受体表达升高(P＜0.01)；与I/R组比较,EI组上述指标降低(P＜0.05),LE组上述指标差异无统计学意义(P＞0.05).结论 乳化异氟醚预处理可减轻大鼠局灶性脑缺血再灌注损伤,其机制与抑制PAF及其受体表达有关.
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血小闆活化因子( PAF)及其受體錶達的影響.方法 健康成年雄性SD大鼠32隻,體重250～300 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)和脂肪乳組(LE組).採用線栓阻塞大腦中動脈2h行再灌註的方法製備大鼠跼竈性腦缺血再灌註損傷模型.于缺血前24h,S組和I/R組腹腔註射生理鹽水10.5 ml/kg,EI組和LE組分彆給予8％乳化異氟醚和30％脂肪乳10.5 ml/kg.再灌註12 h時進行神經功能缺陷評分,隨後每組處死4隻大鼠,採用TTC染色法測定腦梗死體積,每組取其餘4隻大鼠,採集靜脈血樣,採用ELISA法測定血漿PAF濃度,隨後處死大鼠,分離海馬和皮層,採用Western blot法測定PAF受體的錶達.結果 與S組比較,其餘3組神經功能缺陷評分評分、腦梗死體積百分比、血漿PAF濃度、海馬和皮層PAF受體錶達升高(P＜0.01)；與I/R組比較,EI組上述指標降低(P＜0.05),LE組上述指標差異無統計學意義(P＞0.05).結論 乳化異氟醚預處理可減輕大鼠跼竈性腦缺血再灌註損傷,其機製與抑製PAF及其受體錶達有關.
목적 탐토유화이불미예처리대대서국조성뇌결혈재관주시혈소판활화인자( PAF)급기수체표체적영향.방법 건강성년웅성SD대서32지,체중250～300 g,채용수궤수자표법,장대서수궤분위4조(n=8):가수술조(S조)、결혈재관주조(I/R조)、유화이불미조(EI조)화지방유조(LE조).채용선전조새대뇌중동맥2h행재관주적방법제비대서국조성뇌결혈재관주손상모형.우결혈전24h,S조화I/R조복강주사생리염수10.5 ml/kg,EI조화LE조분별급여8％유화이불미화30％지방유10.5 ml/kg.재관주12 h시진행신경공능결함평분,수후매조처사4지대서,채용TTC염색법측정뇌경사체적,매조취기여4지대서,채집정맥혈양,채용ELISA법측정혈장PAF농도,수후처사대서,분리해마화피층,채용Western blot법측정PAF수체적표체.결과 여S조비교,기여3조신경공능결함평분평분、뇌경사체적백분비、혈장PAF농도、해마화피층PAF수체표체승고(P＜0.01)；여I/R조비교,EI조상술지표강저(P＜0.05),LE조상술지표차이무통계학의의(P＞0.05).결론 유화이불미예처리가감경대서국조성뇌결혈재관주손상,기궤제여억제PAF급기수체표체유관.
Objective To investigate the effects of emulsified isoflurane preconditioning on the expression of platelet-activating factor (PAF) and PAF receptor during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-two healthy adult male SD rats weighing 250-300 g were randomly divided into 4 groups ( n =8each):group sham operation (group S); group I/R; group emulsified isoflurane preconditioning( group EI) and group lipid emulsion (group LE).Focal cerebral I/R was induced by 2 h occlusion of middle cerebral artery followed by reperfusion in groups I/R,EI and LE.8％ emulsified isoflurane 10.5 ml/kg and 30％ lipid emulsion 10.5 ml/kg were injected intraperitoneally at 24 h before cerebral ischemia in groups EI and LE respectively.The neurologic deficit score (NDS) (0 =no deficit,4 =unable to control) was evaluated at 12 h of reperfusion.Venous blood samples were collected for measurement of plasma PAF concentration.The animals were then sacrificed and their brains removed for determination of infarct size (by TTC staining) and PAF receptor expression in hippocampus and cerebral cortex (by Western blot).Results Focal cerebral I/R significantly increased NDS,the infarct size,plasma PAF concentration and PAF receptor expression in cerebral cortex and hippocampus in group I/R as compared with group S.Emulsified isoflurane preconditioning significantly attenuated the focal cerebral I/R induced above changes in group EI as compared with group I/R,but there was no significant difference between groups I/R and LE.Conclusion Emulsified isoflurane preconditioning can attenuate focal cerebral I/R injury by inhibiting PAF and PAF receptor expression.
