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brain ischemic reperfusion injury
相关语句
  脑缺血再灌注损伤
     Conclusion: Dexamethasone aggravates brain ischemic reperfusion injury,mannitol is effective for reducing brain ischemia reperfusion injury,and application of the combined agents is the most effective treatment.
     结论 :地塞米松可加重脑缺血再灌注损伤 ,甘露醇具有确切的减轻再灌注脑损伤的作用 ,甘露醇复合地塞米松治疗效果最佳
短句来源
  脑缺血再灌注
     Conclusion: Dexamethasone aggravates brain ischemic reperfusion injury,mannitol is effective for reducing brain ischemia reperfusion injury,and application of the combined agents is the most effective treatment.
     结论 :地塞米松可加重脑缺血再灌注损伤 ,甘露醇具有确切的减轻再灌注脑损伤的作用 ,甘露醇复合地塞米松治疗效果最佳
短句来源
     Objective: To study the effects of Salvia Miltiorrhiza(SM) on neuron apoptosis and expression of Bcl-2 mRNA in hippocampus and dentate gyrus of rat after focal brain ischemic reperfusion injury.
     目的:探讨中药复方丹参对大鼠脑缺血再灌注后海马和齿状回神经细胞凋亡及Bcl-2 mRNA表达的影响。
短句来源
  “brain ischemic reperfusion injury”译为未确定词的双语例句
     Conclusions Aspirin,even at low dose,inhibits the acute inflammation in brain ischemic reperfusion injury,which is related to inhibition of the activity of NF-κB and the expression of TNF-α and IL-1β.
     其机制可能与抑制NF-κB的激活和IL-1β、TNF-α表达有关。
短句来源
     at the 4th week and the 2nd month,it was decreased in each region Conclusions The hippocampal NMDA receptor is related to the cognitive impairment of VD rat model In the early phase of the brain ischemic reperfusion injury,the expression of NMDAR mRNA increase,which mediate the exitotoxicity,but it decrease in the anaphase,which might be correlated to the learning and memory impairment of VD Therefore it supply the foundation to use antagonist or agonist of EAAs receptor in the VD therapy
     结论 大鼠海马区NMDAR与学习记忆有关 ,在脑缺血的早期表达增高介导了兴奋毒性作用 ; 但在缺血后期 ,NMDARmRNA表达减低可能与学习记忆损害有关 ,为进一步进行NMDAR拮抗剂和激动剂治疗VD的研究提供了实验依据。
短句来源
     Methods: Reversible middle cerebral artery occlusion(MCAO) without craniectomy was used to establish model of focal brain ischemic reperfusion injury in rats. TUNEL staining and in situ hybridization were used to detect neuron apoptosis and expression of Bcl-2()mRNA in hippocampus and dentate gyrus of rat; image analysis was also performed.
     方法:采用大脑中动脉内栓线法建立大鼠大脑中动脉缺血再灌注模型,应用原位细胞凋亡检测和原位杂交技术检测大鼠海马和齿状回神经细胞凋亡和Bcl-2 mRNA的表达并做图像分析。
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  相似匹配句对
     Oligodendrocytes and Ischemic Brain Injury
     少突胶质细胞与缺血性脑损伤
短句来源
     Mitochondrion and myocardial ischemic-reperfusion injury
     线粒体与心肌缺血-再灌注损伤
短句来源
     Myocardium Ischemic Preconditioning and Reperfusion Injury
     心肌缺血预适应与再灌注损伤
短句来源
     THE EFFECTS OF CEREBRAL ISCHEMIC DURATION ON BRAIN ACETYLCHOLINESTERASE LEVEL AND REPERFUSION INJURY
     缺血时间对脑缺血再灌注损伤及脑组织AChE表达的影响
短句来源
     The impact of ischemic and reperfusion brain injury on NMR and spectroscopy of the cerebrum and cerebellum in rats
     大鼠脑缺血及再灌注损伤对大小脑核磁共振成像和波谱的影响
短句来源
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Objective To establish a reliable vascular dementia(VD) rat model to study the changes of the NMDAR1mRNA expression in rat's Hippocampus,so as to provide the theoretical basis for the mechanism of NMDAR's effect on cognitive impairment of VD rat model Methods The VD rat model was established by four-vessel occlusion(4VO) The changes of memory ability, LTP and the NMDAR1 mRNA expression in the hippocampus were administered by computerized shuttle training case, extracorporeal hippocampal slices method...

Objective To establish a reliable vascular dementia(VD) rat model to study the changes of the NMDAR1mRNA expression in rat's Hippocampus,so as to provide the theoretical basis for the mechanism of NMDAR's effect on cognitive impairment of VD rat model Methods The VD rat model was established by four-vessel occlusion(4VO) The changes of memory ability, LTP and the NMDAR1 mRNA expression in the hippocampus were administered by computerized shuttle training case, extracorporeal hippocampal slices method and in situ hybridization Results Compared with the control group,the AAR in the VD model group was less in the 2nd week, the 4th week and the 2nd month( P <0 05) It was more obviously at the later two time points( P <0 01) In the slices of extracorporeal hippocampal CA1 region,LTP detection showed that its injury had happened clearly in VD model group at each time point of the 2nd week,the 4th week and the 2nd month Compared with the control group, at the 2nd week the mean optical density (OD) of NMDAR1mRNA expression in pyramidal cell layer of hippocampus in the VD model group was increased in the CA1 and CA3 regions,but no changes were found in DG region; at the 4th week and the 2nd month,it was decreased in each region Conclusions The hippocampal NMDA receptor is related to the cognitive impairment of VD rat model In the early phase of the brain ischemic reperfusion injury,the expression of NMDAR mRNA increase,which mediate the exitotoxicity,but it decrease in the anaphase,which might be correlated to the learning and memory impairment of VD Therefore it supply the foundation to use antagonist or agonist of EAAs receptor in the VD therapy

目的 观察四血管阻断 (4VO)大鼠海马NMDA受体NMDAR的变化规律 ,探讨其在血管性痴呆 (VD)形成中的作用机制。方法 改良的Pulsinelli 4VO法建立大鼠血管性痴呆模型 ;电脑控制的穿梭箱系统和离体海马脑片诱导的CA1区LTP检测大鼠学习记忆 ;原位杂交方法检测大鼠海马NMDAR1mRNA的表达。结果 VD组大鼠的主动回避反应在 2周时较对照组显著下降 (P<0 0 5 ) ,4周和 2月时更加明显 (P <0 0 1) ,海马脑片长时程增强 (LTP)的诱导出现明显障碍 ;VD组 2周时CA1和CA3区NMDAR1mRNA表达较对照组增高 ,DG区无明显改变 ;4周和 2月时海马各区表达均减低。结论 大鼠海马区NMDAR与学习记忆有关 ,在脑缺血的早期表达增高介导了兴奋毒性作用 ;但在缺血后期 ,NMDARmRNA表达减低可能与学习记忆损害有关 ,为进一步进行NMDAR拮抗剂和激动剂治疗VD的研究提供了实验依据。

Objective To evaluate the changes of endoxin during cerebral ischemic reperfusion injury,and the prevention and treatment effect of anti digoxin antiserum(endoxin antagonist)on bilateral cerebral hemisphere ischemic reperfusion inury.Methods The global cerebral ischemic reperfusion model in SD rats was prepared by Kameyamas manner.After ischemia for 30min,reperfusion was established,and different does of anti digoxin...

Objective To evaluate the changes of endoxin during cerebral ischemic reperfusion injury,and the prevention and treatment effect of anti digoxin antiserum(endoxin antagonist)on bilateral cerebral hemisphere ischemic reperfusion inury.Methods The global cerebral ischemic reperfusion model in SD rats was prepared by Kameyamas manner.After ischemia for 30min,reperfusion was established,and different does of anti digoxin antiserum were injected via caudal vein.The blood samples were collected at 60min of reperfusion.The rats were killed,and cerebral hemisphere was removed for preparing homogenate.The levels of serum CK,serum and brain tissue endoxin,brain tissue ATPase activities were examined respectively.Results The levels of serum and brain tissue endoxin in ischemic reperfusion group were significantly higher than those in false operation group,while serum CK activity increased outstandingly,ATPase activity in brain tissue had a significant decrease.Anti digoxin antiserum remarkably decreased the level of brain tissue endoxin and serum CK activity,but made the level of serum endoxin increased significantly.The high and middle concentration of anti digoxin antiserum had a significant effect of raising brain tissue ATPase activity.Conclusion Cerebral ischemic reperfusion could increase the level of brain tissue and serum endoxin.Endoxin is a major factor mediated brain ischemic reperfusion injury.Anti digoxin antiserum can attenuate brain injury and has a protection and treating effect on cerebral ischemic reperfusion injury by antagonizing endoxin. [

目的 观察大鼠脑缺血 再灌注损伤时内洋地黄素水平变化及内洋地黄素拮抗药地高辛抗血清对脑缺血 再灌注损伤的防治作用。方法 采用Kameyama s三动脉夹闭法制作双侧大脑半球缺血模型。缺血 30分钟后再灌注。于再灌注同时 ,尾静脉注射不同剂量内洋地黄素拮抗药地高辛抗血清。再灌注 60分钟后取血分离血清 ,同时断头取脑制作脑匀浆。测定血清CK含量、血清和脑组织内洋地黄素含量以及脑组织ATP酶活性。结果 脑缺血 再灌注时 ,脑组织和血清内洋地黄素水平明显升高 ,血清CK活性显著增高 ,而脑组织ATP酶活性显著下降。地高辛抗血清能显著降低脑组织内洋地黄素水平降低血清CK活性 ,但血清内洋地黄素水平却显著提高 ;大、中剂量地高辛抗血清能明显提高脑组织ATP酶活性。结论 脑缺血再灌注时内洋地黄素水平显著升高 ,内洋地黄素是介导脑缺血 再灌注损伤的重要因子。内洋地黄素拮抗药地高辛抗血清通过拮抗内洋地黄素而减轻脑缺血 再灌注损伤 ,对脑缺血 再灌注损伤具有防治作用

Objective: To determine the effect of dexamethasone and mannitol on reperfusion injury after global brain ischemia in rats.Methods:Forty two Wistar rats were randomly divided into six groups:normal group ( n =5),normal rats without any surgical operation; sham operative group ( n =6), the rat bilateral vertebral arteries were electrocauterized; ischemia group ( n =7), bilateral vertebral arteries were electrocauterized, and both carotid arteries were occluded temporarily by atraumatic...

Objective: To determine the effect of dexamethasone and mannitol on reperfusion injury after global brain ischemia in rats.Methods:Forty two Wistar rats were randomly divided into six groups:normal group ( n =5),normal rats without any surgical operation; sham operative group ( n =6), the rat bilateral vertebral arteries were electrocauterized; ischemia group ( n =7), bilateral vertebral arteries were electrocauterized, and both carotid arteries were occluded temporarily by atraumatic artery clasp for 10 minutes; dexamethasone group ( n =8), intraperitoneal dose of dexamethasone of 10 mg·kg -1 (body weight)was received immediately after vessel occlusion (VO), twice a day; mannitol group ( n =8),intravenous dose of 20% mannitol of 10 ml·kg -1 was received 4 hours after VO,three times a day; dexamethasone combined with mannitol group ( n =8),both intraperitoneal dexamethasone of 10 mg·kg -1 , twice a day, and intravenous 20% mannitol of 10 ml·kg -1 , three times a day were administered. All rats were sacrificed and brains were removed after 72 hours. A 3 mm thick coronal brain was sliced from temporal lobe for histopathological examination. Ischemic neurons and neuron density in hippocampal CA1 region were measured with paraffin sections stained by HE methods. Apoptosis of cells was observed by TUNEL method.The rest of the brain was used to measure water contents by means of wet-dry method. Results: All drug treated groups could effectively reduce brain edema. Dexamethasone exacerbated ischemic neuronal injury but dexamethasone combined with mannitol was the most effective treatment for brain ischemia injury compared with other groups. Conclusion: Dexamethasone aggravates brain ischemic reperfusion injury,mannitol is effective for reducing brain ischemia reperfusion injury,and application of the combined agents is the most effective treatment.

目的 :观察地塞米松、甘露醇对缺血再灌注损伤脑组织的作用。方法 :Wistar大鼠 4 2只 ,随机分为 6组 ,正常对照组 (n =5 ) ;假手术组 (n =6 ) ,仅电凝双侧椎动脉 ;缺血对照组 (n =7) ,电凝双侧椎动脉 ,夹闭双侧颈总动脉 10min后恢复脑血流灌注 ;地塞米松治疗组 (n =8) ,脑缺血复灌后腹腔注射地塞米松 10mg·kg-1,每日 2次 ;甘露醇治疗组 (n =8) ,脑缺血复灌后尾静脉注射 2 0 % (体积分数 )甘露醇 10ml·kg-1,每日 3次 ;地塞米松复合甘露醇治疗组 (n =8)脑缺血复灌后腹腔注射地塞米松 10mg·kg-1,每日 2次 ,同时给予 2 0 %甘露醇 10ml·kg-1,尾静脉注射 ,每日 3次。 6组均于 72h后断头取脑 ,于颞叶最宽处切取 3mm厚冠状面脑组织切片 ,行病理HE染色和TUNEL染色 ,计数海马区神经元密度和缺血细胞。其余脑组织行干—湿称重法测脑水含量。结果 :各药物处理组均能有效减轻脑水肿。与其他处理组比较 ,地塞米松处理组缺血性脑损伤表现最严重 ,而在地塞米松复合甘露醇处理组脑损伤表现最轻。结论 :地塞米松可加...

目的 :观察地塞米松、甘露醇对缺血再灌注损伤脑组织的作用。方法 :Wistar大鼠 4 2只 ,随机分为 6组 ,正常对照组 (n =5 ) ;假手术组 (n =6 ) ,仅电凝双侧椎动脉 ;缺血对照组 (n =7) ,电凝双侧椎动脉 ,夹闭双侧颈总动脉 10min后恢复脑血流灌注 ;地塞米松治疗组 (n =8) ,脑缺血复灌后腹腔注射地塞米松 10mg·kg-1,每日 2次 ;甘露醇治疗组 (n =8) ,脑缺血复灌后尾静脉注射 2 0 % (体积分数 )甘露醇 10ml·kg-1,每日 3次 ;地塞米松复合甘露醇治疗组 (n =8)脑缺血复灌后腹腔注射地塞米松 10mg·kg-1,每日 2次 ,同时给予 2 0 %甘露醇 10ml·kg-1,尾静脉注射 ,每日 3次。 6组均于 72h后断头取脑 ,于颞叶最宽处切取 3mm厚冠状面脑组织切片 ,行病理HE染色和TUNEL染色 ,计数海马区神经元密度和缺血细胞。其余脑组织行干—湿称重法测脑水含量。结果 :各药物处理组均能有效减轻脑水肿。与其他处理组比较 ,地塞米松处理组缺血性脑损伤表现最严重 ,而在地塞米松复合甘露醇处理组脑损伤表现最轻。结论 :地塞米松可加重脑缺血再灌注损伤 ,甘露醇具有确切的减轻再灌注脑损伤的作用 ,甘露醇复合地塞米松治疗效果最佳

 
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