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reversible focal
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     Influences of ginsenosides Rb1 and Rg1 on reversible focal brain ischemia in rats
     人参皂苷Rb_1和Rg_1对大鼠可逆性局灶性脑缺血的影响(英文)
短句来源
     The synergistic neuroprotective effects by combining isoflurane preconditioning with Shenfu injection(参附注射液) in rats subjected to reversible focal cerebral ischemia injury
     异氟醚预处理联合参附注射液对大鼠短暂性局灶性脑缺血损伤协同保护作用的研究
短句来源
     Evaluation of the modified model of reversible focal cerebral ischemia in rats by MRI
     MRI评价改进的大鼠可逆性局灶性脑缺血模型
短句来源
     Research on the model of reversible focal cerebral ischemia by occlusion of the middle cerebral artery in rats
     大鼠大脑中动脉阻断可逆性局灶脑缺血模型的研究
短句来源
     Objective To study the effect of dopamine D1 receptor antagonist SCH 23390 and D2 receptor antagonist Eticlopride on infarct volume and regional cerebral blood flow(rCBF) in cortical penumbra during reversible focal cerebral ischemia in rats.
     目的 研究多巴胺 (DA)D1受体拮抗剂SCH 2 3390和D2受体拮抗剂Eticlopride对可逆性局灶性脑缺血梗塞体积及皮层半暗带脑血流的影响。
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  “reversible focal”译为未确定词的双语例句
     The spatiotemporal relationship of neuronal cell DNA damage and apoptosis after reversible focal cerebral ischemia in rats
     脑缺血再灌注大鼠神经细胞DNA损伤与凋亡的时空关系分析
短句来源
     Methods: 2 hours of reversible focal ischemia in rats were produced by improved the method of Connolly' suture occlusion of MCA and the expression of SAMDC-mRNA in the cortex and subcortex was measured by RT-PCR after 2,4,8 and 24h reperfusion following 2h ischemia respectively. The time courses of SAMDC-mRNA expression in the experimental and control group were analyzed.
     方法:在Connolly线栓法的基础上进行改良,复制大鼠MCA区2h脑缺血-再灌流2,4,8,24h动物模型,用逆转录多聚酶链反应(RT-PCR)测定缺血区皮质和皮质下组织不同时相SAMDC-mRNA的表达。
短句来源
     Using the rat model of reversible focal cerebral ischemia,we studied the changes of cerebral infarction size,brain water content,energy metabolism,MDA and SOD in rats subjected to 6 or 9 hr of permanent cerebral ischemia and 6 hr of cerebral ischemia followed by 3 hr of reperfusion.
     采用大鼠局部脑缺血再灌流模型,研究了大鼠脑缺血6h、9h和缺血6h再灌流3h脑梗塞体积,脑含水量,能量代谢,丙二醛(MDA)和超氧化物歧化酶(SOD)的变化。
短句来源
     Methods A stable and reversible focal ischemia model with unilateral middle cerebral artery occlusion was established and evaluated by CT perfusion imaging and TTC staining.
     方法利用线栓法建立大鼠急性脑缺血再灌注模型,并通过其CT灌注扫描图像与脑切片TTC染色图像相比较对模型进行评价。
短句来源
     Analysis and Comparsion of Apoptosis or Necrosis After Reversible Focal Cerebral Ischemia
     局灶性脑缺血神经元凋亡和坏死的分析比较
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  相似匹配句对
     A modified model of reversible focal cerebral ischemia in rats
     栓线法制作局灶性大鼠脑缺血再灌注模型的改进及效果
短句来源
     1: focal ;
     局部分布,为1级;
短句来源
     Improvement of development of the model of reversible focal cerebral ischemia of rats.
     大鼠可逆性局灶性脑缺血模型复制方法的改进
短句来源
     Reversible Renascence
     可逆转性的重生
短句来源
     Reversible Thermochromism Materials
     可逆热致变色材料
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  reversible focal
Caspase-9 Inhibition after Focal Cerebral Ischemia Improves Outcome following Reversible Focal Ischemia
      
Spatial and temporal changes in tissue pH and ATP distribution in a new model of reversible focal forebrain ischemia in the rat
      
Ultrastructural Morphology of Neuronal Death Following Reversible Focal Ischemia in the Rat
      
A detailed description is given of a new model of reversible focal cerebral ischaemia in rats.
      
The reversible focal MRI abnormalities in complex partial seizure: technical instruction
      
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Objective The aim of the present study is to compare the effects of mild hypothermia induced in different courses in the rats subjected to 3 hours of middle cerebral artery occlusion followed by 72 hours of reperfusion. Methods Thirty-two male SD rats were divided into three mild hypothermic groups according to the duration of the mild hypothermia (MHT 32±0 2 ℃), which including intra ischemia(MHTi), intra reperfusion (MHTp), intraischemia/reperfusion(MHTi+p) group, and...

Objective The aim of the present study is to compare the effects of mild hypothermia induced in different courses in the rats subjected to 3 hours of middle cerebral artery occlusion followed by 72 hours of reperfusion. Methods Thirty-two male SD rats were divided into three mild hypothermic groups according to the duration of the mild hypothermia (MHT 32±0 2 ℃), which including intra ischemia(MHTi), intra reperfusion (MHTp), intraischemia/reperfusion(MHTi+p) group, and one normothermic group (NT 37±0 2 ℃) as control. Reversible focal ischemia was carried out in rats with suture model. The infarct volume stained by 2% 2, 3, 5-triphenyltetrazolium chlorides was measured at 72 hours after reprefusion to determine the effects of MHT. Results Compared to the NT rats, the infarct volume was significantly reduced in both MHTi and MHTi+p groups ( P <0 05), especially in the latter. The protective effect of MHTp is limited. Conclusions This study demonstrated that MHTi+p group has more substantial protective effects on reducing ischemia/reperfusion injury than MHTi group which suggested that ischemic and reperfusional injuries were an ongoing process and the concept of a therapeutic window must be considered not only the intiating time of mild hypothermia but also the duration of the intervention.

目的 研究缺血期、再灌注期、缺血持续至再灌注期亚低温对脑缺血再灌注损伤的作用。  方法  3 2只雄性SD鼠采用线段阻塞大脑中动脉的可逆性局灶脑缺血模型 ,缺血 3小时再灌注 72小时后计算各组脑梗塞灶体积。  结果 再灌注后诱导亚低温的治疗作用是有限的 ,缺血期 ,尤其是缺血期持续至再灌注期亚低温能明显减轻脑缺血损伤。  结论 脑缺血再灌注损伤是一个缓慢进展的过程 ,亚低温治疗不但要考虑到低温诱导的时间 ,其持续时间的长短也很重要

Using the rat model of reversible focal cerebral ischemia,we studied the changes of cerebral infarction size,brain water content,energy metabolism,MDA and SOD in rats subjected to 6 or 9 hr of permanent cerebral ischemia and 6 hr of cerebral ischemia followed by 3 hr of reperfusion.The results showed that the severe cerebral infarction size and  brain edema were caused,the content of ATP and the activity of SOD significantly decreased, the content of lactate and MDA significantly increased in the two permanent...

Using the rat model of reversible focal cerebral ischemia,we studied the changes of cerebral infarction size,brain water content,energy metabolism,MDA and SOD in rats subjected to 6 or 9 hr of permanent cerebral ischemia and 6 hr of cerebral ischemia followed by 3 hr of reperfusion.The results showed that the severe cerebral infarction size and  brain edema were caused,the content of ATP and the activity of SOD significantly decreased, the content of lactate and MDA significantly increased in the two permanent ischemia groups compared with the control group(P<0.05 or P<0.001). The changes of cerebral infarction size and brain edema  were not significantly different(P>0.05) between the reperfusion group and the permanent ischemia groups. Our present data indicated that 6 hr of cerebral ischemia could induce severe brain damage,after then,the evolution of brain injury tended to be slow with increasing ischemic time.The reperfusion injury was not significant in this study.

采用大鼠局部脑缺血再灌流模型,研究了大鼠脑缺血6h、9h和缺血6h再灌流3h脑梗塞体积,脑含水量,能量代谢,丙二醛(MDA)和超氧化物歧化酶(SOD)的变化。结果:脑缺血6h、9h可以造成严重的脑梗塞和脑水肿,ATP含量和SOD活性显著降低,乳酸和MDA含量显著增加,和对照组相比均有显著差异(P<0.05或P<0.001)。再灌组和缺血两组比较,脑梗塞体积,脑水肿无明显差别(P>0.05),ATP、乳酸、SOD和MDA均有不程度的改善。提示,大鼠局部脑缺血超过6h可造成严重的脑损伤,并随缺血时间的再延长,脑损伤变化趋于平缓。再灌后,脑损伤未见明显加重。

To evaluate the dynamic changes of NOS activity and JCBF during the cerebral ichemia and reperfusion in rats. Using modified Koizumi's rat reversible focal cerebral ischemia model ,we have examined the time course of NOS activity of the ischemic brain by the Bredt and Snyder's method and the penumbra ICBF with LDF. The ischemic brain NOS activity increase 2~3 folds at 10 mm of ishcemia (P<0. 01), and then decreased dramatically to the baseline at 90 min(P<0. 05). During the reperfusion, it increased again...

To evaluate the dynamic changes of NOS activity and JCBF during the cerebral ichemia and reperfusion in rats. Using modified Koizumi's rat reversible focal cerebral ischemia model ,we have examined the time course of NOS activity of the ischemic brain by the Bredt and Snyder's method and the penumbra ICBF with LDF. The ischemic brain NOS activity increase 2~3 folds at 10 mm of ishcemia (P<0. 01), and then decreased dramatically to the baseline at 90 min(P<0. 05). During the reperfusion, it increased again with a peak at 10 mm(vs. preisehemia, P<0. 05) ,and returned to the baseline at 90 min. The ICBF rose to 30% of baseline at 10~20 min of ischemia(P<0. 05). At 10 mm of reperfusion ICBF return to over 100% of baseline(P>0. 05) ,and reduced rapidly 30 mm later. In the early stage of the ischemia, influx of Ca2+ activates NOS leading to the increase of NO production. It maybe helpful to maintaining the remaining CBF of the ischemic territory and the penumbra. During the reperfusion, with increased expression and Ca2+ overload, NOS activity increases again. Increased NO reacts with O2 which generates many toxic free radicals result in the cell damage.

研究局灶性脑缺血和再灌注期一氧化氮合酶的活性和局部脑血流量的动态变化.用改良Koizumi’s大鼠局灶性脑缺血和再灌注模型及改良Bredt和Snyder’s法测定了缺血和再灌注期缺血侧脑组织一氧化氮合成酶(NOS)总活性,并同步以激光多普勒血流仪(LDF)对缺血周边区局部脑血流量(ICBF)进行了测定.结果:缺血早期,缺血侧半球脑组织NOS活性急剧升高至缺血前2~3倍(P<0.01),缺血后期NOS活性降至缺血前水平(P>0.05);缺血10~20 min缺血周边区ICBF回升至缺血前的30%左右(P<0.05);再灌注10min出现高灌,30min后持续下降.提示:缺血期因为钙内流,使NOS活性剧增,有利于维持缺血区和周边区的脑血流量,但过量产生的NO可造成细胞损伤.再灌注期由于表达增加,加之钙超载使NOS活性再度升高,NO可与再灌注期大量产生的超氧阴离子反应生成毒性自由基而损伤细胞.

 
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