CAJ | 학술논문

目的评价七氟醚麻醉对局灶性脑缺血再灌注大鼠脑组织水通道蛋白9( AQP-9)表达的影响.方法成年雄性SD大鼠75只,体重230～270 g,采用随机数字表法,将其随机分为3组(n=25):假手术组(S组)、缺血再灌注组(UR组)和七氟醚麻醉组(SE组).S组和I/R组静脉注射芬太尼10μg/kg后静脉输注芬太尼25μg·kg-1·h-1,吸入65％N2O和35％O2；SE组吸入2.0％七氟醚和35％ O2.I/R组和SE组采用线栓法制备大鼠局灶性脑缺血再灌注模型,缺血2h后恢复灌注.分别于再灌注6h、1、2、3和5d时测定神经功能缺陷评分和脑组织AQP-9表达,计算脑肿胀率.结果与S组比较,I/R组和SE组再灌注6h、1、2、3和5d时神经功能缺陷评分升高,再灌注1、2、3d时脑肿胀率升高,再灌注1、2、3和5d时脑组织AQP-9表达上调(P＜0.05)；与I/R组比较,SE组再灌注2和3d时神经功能缺陷评分下降,脑肿胀率降低,再灌注2、3和5d时脑组织AQP-9表达上调(P＜0.05).结论七氟醚麻醉减轻大鼠局灶性脑缺血再灌注损伤的机制与上调脑组织AQP-9的表达有关.
목적 평개칠불미마취대국조성뇌결혈재관주대서뇌조직수통도단백9( AQP-9)표체적영향.방법 성년웅성SD대서75지,체중230～270 g,채용수궤수자표법,장기수궤분위3조(n=25):가수술조(S조)、결혈재관주조(UR조)화칠불미마취조(SE조).S조화I/R조정맥주사분태니10μg/kg후정맥수주분태니25μg·kg-1·h-1,흡입65％N2O화35％O2；SE조흡입2.0％칠불미화35％ O2.I/R조화SE조채용선전법제비대서국조성뇌결혈재관주모형,결혈2h후회복관주.분별우재관주6h、1、2、3화5d시측정신경공능결함평분화뇌조직AQP-9표체,계산뇌종창솔.결과 여S조비교,I/R조화SE조재관주6h、1、2、3화5d시신경공능결함평분승고,재관주1、2、3d시뇌종창솔승고,재관주1、2、3화5d시뇌조직AQP-9표체상조(P＜0.05)；여I/R조비교,SE조재관주2화3d시신경공능결함평분하강,뇌종창솔강저,재관주2、3화5d시뇌조직AQP-9표체상조(P＜0.05).결론 칠불미마취감경대서국조성뇌결혈재관주손상적궤제여상조뇌조직AQP-9적표체유관.
Objective To investigate the effects of sevoflurane anesthesia on aquaporin-9 (AQP-9) expression in brain tissue after focal cerebral ischemia-reperfusion (I/R) in rats.Methods Seventy-five male SD rats weighing 230-270 g were randomly divided into 3 groups ( n =25 each):group sham operation (group S) ; group I/R and group sevoflurane anesthesia (group SE).All the animals were tracheally intubated under 2.0％ sevoflurane and mechanically ventilated.Anesthesia was maintained with fentanyl infusion at 25 μg· kg-1 · h-1 after a bolus of fentanyl 10 μg/kg and inhalation of 65％ N2O in O2 in groups S and I/R and with inhalation of 2％ sevoflurane in 35％ O2 in group SE.Focal cerebral ischemin was induced by occlusion of middle cerebral artery for 2 h using a nylon thread with rounded tip which was inserted into the right internal carotid artery and advanced cranially until resistance was met.The neurologic function was assessed and scored (0=no deficit,4 =unable to move,unconscious) and brain edema rate (volume of ischemic hemisphere-volume of contralateral hemisphere ÷volume of contralateral hemisphere × 100％ ) and expression of AQP-9 were determined at 6 h,1,2,3 and 5 d of reperfusion.Results Focal cerebral I/R significantly increased neurologic deficit scores,brain edema rate and AQP-9 expression in brain tissue in group I/R as compared with group S.Sevoflurane anesthesia significantly attenuated the I/R-induced increase in neurologic deficit scores and brain edema rate and further increased I/R-induced increase in AQP-9 expression in brain tissue.Conclusion Sevoflurane anesthesia can reduce focal cerebral I/R injury by up-regulating the expression of AQP-9 in brain tissue.