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acute brain ischemia
相关语句
  急性脑缺血
     Methods: Establish the rat acute brain ischemia model with 42 male SD rats (280 - 320g) divided randomly into operation group (A1,n=28) and non - operation group (A2,n=14).
     方法:建立大鼠急性脑缺血模型,选用42只雄性SD大鼠(280-320g),随机分为手术组(A1组,n=28)、假手术组(A2组,n=14)。
     2. Using DWI, PWI techniques on rat acute brain ischemia reperfusion model to discuss and study the etiology of brain ischemia.
     2.利用DWI及PWI研究大鼠(MCAO)急性脑缺血再灌注模型,观察脑缺血再灌注的动态变化规律,探讨急性脑缺血的发病机理。
短句来源
     It was found that all the three experimental groups showed significant increase in survival time after sodium nitrite poisoning compared with the control group (P<0.01), and the groups with doses of 1.68 and 2.52 g/kg BW d -1 showed increase in survival time after acute brain ischemia compared with the control group(P<0.05).
     结果表明:与对照组比较,3个剂量组亚硝酸钠中毒存活时间明显延长(P<0.01),1.68、2.52gkgBWd-1剂量组急性脑缺血性耐缺氧时间也明显延长(P<0.05)。
短句来源
     Rabbit acute brain ischemia reperfusion model was used to investigate the effects of DDPH on the contents of brain Ca 2+ ,Na +,K +, nitric oxide synthase (NOS) and malonaldehyde (MDA) during brain ischemia reperfusion. It was found that intravenous injection of DDPH in a dose of 8 mg/kg before ischemia could significantly reduce the activity of NOS, decrease the contents of MDA and ischemia induced brain Ca 2+ and Na +.
     采用家兔急性脑缺血及缺血再灌注模型 ,观察了 DDPH对缺血及缺血复灌时脑组织内 Ca2 +,Na+,K+等离子及 NOS(一氧化氮合酶 )与 MDA(丙二醛 )含量的影响 ,实验发现 DDPH8mg/ kg于缺血前静脉注射 ,可明显降低NOS的活性 ,减少 MDA的含量 ,并可减少由缺血所致脑组织内 Ca2 +,Na+等离子的含量。
短句来源
     By means of an animal centrifuge,we set up a model of acute brain ischemia resulting from +Gz exposures,using immunohistochemistry after repeated +Gz exposuresto detect the expression of GFAP in hippocampal astrocytes at different times.
     采用动物离心机,建立+Gz引发急性脑缺血模型; 应用免疫组织化学技术,分别检测+Gz重复暴露后不同时间,海马星形胶质细胞GFAP的表达状况。
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  “acute brain ischemia”译为未确定词的双语例句
     Background The main factors which influence the survival rate in acute brain ischemia are ischemic brain edema and hemorrhagic transformation(HT) of the infarction.
     背景影响急性期缺血生存的主要因素是缺血性脑水肿,其次是梗死出血性转化(HT),溶栓治疗可能增加HT发生的机会,这些病变的关键环节都与血脑屏障(BBB)开放或破坏有关。
短句来源
     CONCLUSION: Doxepin decreases the contents of Ca 2+ ,Na +, H 2O in brain tissue with acute brain ischemia_reperfusion injury markedly. It displays the effects of calcium antagonism.
     结论:多塞平能显著降低因缺血引起的脑组织Ca2+,Na+,H2O含量增高,表现出钙拮抗作用
短句来源
     The concentration of cAMP, cGMP and A Ⅱ in the b-rain and plasma were detected at control, acute brain ischemia and lien zhong' Point acupnnctured.
     分别测定正常,夹闭时和针刺“人中”穴后家兔脑及血浆中cAMP、cGMP和AⅡ含量。
短句来源
     3 P selectin was involved in the ischemic injury . Maybe blocking the P selectin's function is a new therapy for acute brain ischemia.
     3、P选择素参与了脑缺血损伤过程,阻断P选择素的作用将为脑血管病的治疗提供新途径。
短句来源
     Conclusion:YiQiHuoXue concoction could improved the stress ability of nerve cells of acute brain ischemia by enhance the content of c-fos protein,it implied that herb concoction has a good prospect in the area of treating brain occlusion.
     结论:益气活血汤可通过提高缺血区c-fos蛋白的含量改善神经细胞的应激能力,提示了中药复方治疗脑梗死的应用前景。
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  相似匹配句对
     The Neuroprotective Effect of G-CSF in Acute Brain Ischemia
     粒细胞集落刺激因子在急性脑缺血中的神经保护作用的研究
短句来源
     Acute myocardial ischemia
     心肌缺血
短句来源
     Effect of the acute cerebral ischemia on Ach and ChAT in brain
     急性脑缺血对脑内乙酰胆碱和胆碱乙酰转移酶的影响
短句来源
     HEMORHEOLOGICAL CHANGE AND THE PATHOGENESIS OF EXPERIMENTAL ACUTE BRAIN ISCHEMIA
     实验性脑缺血急性期血液流变学指标改变及机制探讨
短句来源
     STUDIES OF 31 P MRS OF MOUSE BRAIN DURING ACUTE ISCHEMIA
     小鼠大脑急性缺血过程中~(31)PNMR研究
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  acute brain ischemia
All attempts to reduce neuronal damage after acute brain ischemia by the use of neuroprotective compounds have failed to prove efficacy in clinical trials so far.
      
To simulate acute brain ischemia, cytotoxic hypoxia was induced by sodium cyanide or by iodoacetate and excitotoxicity by L-glutamate.
      
Cerebrolysin was shown to protect against MAP2 loss in primary embryonic chick neuronal cultures after brief histotoxic hypoxia and in a rat model of acute brain ischemia.
      
Acute brain ischemia is accompanied by the intense apoptotic and/or necrotic death of cortical neurons.
      
It is demonstrated that ammonium succinate is capable of increasing the survival of rats with acute brain ischemia.
      
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The changes ofCaM contents , distribution and ultrastructure in acute brain ischemia were investigated by immunogold staining (IGS) and enzyme-linked immuno-sorbent assay (ELISA). The ELISA resulls showed that the contents of CaM decreased by 25 and 45% at 10 and 30 min after ischemia, respectively. The numbers of immunogold particle in each field of vision decreased significantly from 9.95 + 3.76 to 5.32+2.44 after 30 min of isch-emia(p<0.001).After 30 min of ischemia, the degranulation of...

The changes ofCaM contents , distribution and ultrastructure in acute brain ischemia were investigated by immunogold staining (IGS) and enzyme-linked immuno-sorbent assay (ELISA). The ELISA resulls showed that the contents of CaM decreased by 25 and 45% at 10 and 30 min after ischemia, respectively. The numbers of immunogold particle in each field of vision decreased significantly from 9.95 + 3.76 to 5.32+2.44 after 30 min of isch-emia(p<0.001).After 30 min of ischemia, the degranulation of the RER and the increase of the matrix density in the Mit were observed by electron mic roscopy.

用ELISA和免疫胶体金标记电镜技术,研究了蒙古沙土鼠急性脑缺血CaM的含量、分布和亚细胞形态结构变化。ELISA测定结果;缺血10分钟,CaM下降25%;缺血30分钟,CaM下降45%。免疫胶体金检查:正常组每个视野胶体金颗粒数为9.95±3.76,缺血组为5.32±2.44,两组相比,P值<0.001。电镜下可见缺血神经元粗面内质网脱颗粒,线粒体基质密度增加等改变。

The acute brain ischemia was formed by ligation ofboth common corotid arteries of the Mongolian gerbil andthe actvities of CaM dependent protein kinase Ⅱ and CaM dependent protein phosphatase were measured in differentischemic time.The results indicated that the activity ofCaM-PKⅡ was susceptible to ischemia.After 5,10,20and 30 minutes of ischemia,the means of the enzymeactivity in each ischemic groups were significantly lowerthan that in control group,the CaM-PrP activity did notchange significantly...

The acute brain ischemia was formed by ligation ofboth common corotid arteries of the Mongolian gerbil andthe actvities of CaM dependent protein kinase Ⅱ and CaM dependent protein phosphatase were measured in differentischemic time.The results indicated that the activity ofCaM-PKⅡ was susceptible to ischemia.After 5,10,20and 30 minutes of ischemia,the means of the enzymeactivity in each ischemic groups were significantly lowerthan that in control group,the CaM-PrP activity did notchange significantly after ischemia.

本文报导了蒙古沙土鼠双侧颈总动脉结扎造成急性脑缺血在不同时间内钙调素依赖性蛋白激酶Ⅱ(CaM—PKⅡ)和钙调素依赖性蛋白磷酸酶(CaM—PrP)活性的变化。结果显示 CaM—PKⅡ活性对脑缺血非常敏感,缺血5分钟、10分钟、20分钟和30分钟各组 CaM—PKⅡ活性均值均显著低于对照组,而 CaM—PrP 活性对脑缺血不敏感。探讨了 CaM—PKⅡ活性降低的可能机制。

The changes of Na,K-ATPase activities in the cerebral tissue in get-bils after acute brain ischemia treated with hyperbaric oxygen (HBO) were investigated.The results showed that Na,K-ATPase activity in cerebral tissue was significantly re- duced (P<0.01) after 60 min ischemia and 80 min reperfusion of the brain.The ani-mals were in comatous and hypoactive state.Convulsion and seizures occurred occasional-ly.After treatment with 101.3 kPa or 253.25kPa pure oxygen,the activity of Na,K-ATPase...

The changes of Na,K-ATPase activities in the cerebral tissue in get-bils after acute brain ischemia treated with hyperbaric oxygen (HBO) were investigated.The results showed that Na,K-ATPase activity in cerebral tissue was significantly re- duced (P<0.01) after 60 min ischemia and 80 min reperfusion of the brain.The ani-mals were in comatous and hypoactive state.Convulsion and seizures occurred occasional-ly.After treatment with 101.3 kPa or 253.25kPa pure oxygen,the activity of Na,K-ATPase increased to approximately the normal value,(no significant difference between101.3 and 253.25kPa).The results indicated that the mechanism of HBO in treatingcerebral edema in gerbils might be closely related to the recovery of Na,K -ATPase ac-tivity in cerebral tissues.

利用蒙古种沙土鼠(Mongolian Gerbil)制成急性脑缺血动物模型,观察了缺血后再灌注及不同氧压的高压氧治疗后脑组织Na,K-ATP 酶活力的改变。结果表明:脑缺血60min 后重灌流80min 的动物呈现昏迷、少动状态,时而出现四肢抽搐、强直等症状;肌力、肌张力下降,并逐渐加重;脑组织Na,K-ATP 酶活力显著下降(P0.01)。以101.3kPa 纯氧和253.25kPa 纯氧治疗缺血60min 动物,脑组织Na,K-ATP 酶活力的恢复,与不治疗组相比,差别非常显著(P<0.01)。其中,又以后者更好,其值已接近正常组(P>0.05)。动物经253.25kPa 治疗后,肌力、肌张力有所恢复,在舱内爬行;其它几组动物的行为无明显改善。提示,高压氧治疗脑水肿机制之一是通过恢复脑组织Na,K-ATP 酶活力,恢复细胞内外离子分布而实现。

 
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