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ischemic damage
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  缺血性损伤
    Conclusions FAP-1 in cerebal tissue of cerebral ischemic rats is over expression. It can show ischemic damage of brain.
    结论缺血性脑梗死大鼠脑组织的FAP-1表达明显增高,其表达增高可以提示脑组织有缺血性损伤
短句来源
    In contrast, much less attention has focused on the ischemic damage to glial cells.
    尽管缺血性神经元损伤的病理生理学机制已经得到了深入研究,但神经胶质细胞的缺血性损伤却很少受到关注。
短句来源
    Discuss:The cerebral white matter damage were very often seen in clinical practice and related with the selective and vulnerable to ischemic damage .
    脑白质的不可逆损伤可破坏信号传递,从而对中枢神经系统(CNS)的整体功能造成严重影响。 脑白质损伤与智能损害相关,是卒中和智能损害的重要危险因素,因此研究脑白质的缺血性损伤对LA具有重要意义。
短句来源
    Methods:K + channel openers (KCOS) were administered intraventricularly 30 min before the occlusion of right middle cerebral artery, the ischemic damage of brain was measured by histopathological examination.
    方法 :于右大脑中动脉夹闭前 3 0min ,向鼠的侧脑室内注射K+ 通道开放剂 ,并应用生理病理学方法检测脑的缺血性损伤情况。
短句来源
    Many experiments indicated that the mechanism of Ischemic cerebrovascular damage was very complicated. In the process of Ischemic damage, besides lack of oxygen and energy metabolization wane, a series of waterfall effects resulting from ischemia are the important factors which cause ischemic neuron necrosis.
    大量的实验研究表明,脑缺血再灌注损伤对脑损害的机制是非常复杂的,在缺血性损伤过程中除缺氧和能量代谢衰竭外,由缺血诱导的一系列瀑布样效应是导致缺血性神经元死亡的重要机制.
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  缺血性损害
    Pathological and experimental studies have indicated thatthe reduction of local cerebral blood flow and progressive ischemic damage oftissue occurred in regions surrounding a hematoma after ICH. The secondarybrain injury is key for prognosis after ICH.
    研究发现,脑出血后脑组织存在广泛的局部血流量降低和缺血性损害,这种继发性损害对脑出血的预后起重要作用。
短句来源
    It may play a beneficial role in salvaging neuronal cells from ischemic damage to intervene the mechanism of apoptosis as soon as possible up to 24 h after reperfusion.
    再灌流后24h内尽早干预细胞凋亡机制的发生仍可能更进一步挽救缺血性损害的神经细胞。
短句来源
    Bax is a pro - apoptotic member of the bcl - 2 family, the expression of protein bax represent cell apoptosis. Cell can apoptosis in the induction of excited amino acid and ischemic damage.
    Bax是Bcl-2家族中一种促凋亡分子,Bax蛋白的表达在很大程度上代表了细胞凋亡的趋势,细胞在各种引发凋亡的信号如兴奋性氨基酸和缺血性损害的刺激下易于发生凋亡。
短句来源
    Results: PSM significantly improved the spatial memory of rats withleft temporal ischemia. RSM reduced the ischemic damage and down-regulated the expression of c-Jun, bFGF andHSP7o.
    结果:经丹参治疗,颞叶缺血性损害大鼠的空间记忆障碍得到显著改善,颞叶缺血损害程度显著减轻,缺血灶内c-Jun、bFGF和HSP70表达明显减少。
短句来源
    Conclusion: NOS positive cells are relatively tolerate to ischemic damage and apoptosis is the major manner of their death.
    结论 :NADPH d阳性神经元对缺血性损害相对耐受 ,细胞凋亡可能为其主要死亡方式。
短句来源
  “ischemic damage”译为未确定词的双语例句
    Study on the Molecular Mechanism of Brain Ischemic Damage by Cerebral Vasospasm the Effects of Tetrandrine in Rabbits
    实验性蛛网膜下腔出血脑血管痉挛后缺血性脑损害的发病机理及粉防己碱的干预作用研究
短句来源
    EXPERIMENTAL STUDY ON BRAIN ISCHEMIC DAMAGE
    尼莫地平对缺血性脑损害的实验研究
短句来源
    Experimental studies on cerebral ischemic damage following unilateral carotid occlusion and the protective effect of 764-3 in rats
    大鼠单侧颈动脉阻断所致的脑缺血性损害和764-3脑保护作用的实验研究
短句来源
    Application development of antagonists of N-methyl-D -aspartate acceptor on brain ischemic damage
    N-甲基-D-天冬氨酸受体拮抗剂类药物在脑缺血损伤中的应用进展
短句来源
    Effects of neurotrophic factors on ischemic damage and the regulation by medicines
    神经营养因子对缺血性脑损伤的影响及其药物调节
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  ischemic damage
In the myocardium without signs of ischemic damage, stimulation of the α1-receptors caused a slowly developing single-phase positive inotropic response.
      
Structural ischemic damage was more pronounced in patients with severe hypertrophy and structural reconstitution was delayed.
      
Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.
      
Dexamethasone also reduced the extent of ischemic damage as assessed by a nitro-blue tetrazolium staining technique, providing anatomic verification of the reduced ischemic damage.
      
The role of lipid peroxidation in pathogenesis of ischemic damage and the antioxidant protection of the heart
      
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The contents of Malondialdehyde(MDA) and Superoxide dismutase (SOD) were measured in the brain and blood of 45 rabbits. The epileptic seizures and pathological changes were observed to study the relationship between different levels of blood pressure and the generation of free radicals and their influence to brain damage during reperfusion. Results showed that the post-ischemic damage of brain became worse and free radicals' generation most markedly increased in moderately and extremely hyper-tensive groups,...

The contents of Malondialdehyde(MDA) and Superoxide dismutase (SOD) were measured in the brain and blood of 45 rabbits. The epileptic seizures and pathological changes were observed to study the relationship between different levels of blood pressure and the generation of free radicals and their influence to brain damage during reperfusion. Results showed that the post-ischemic damage of brain became worse and free radicals' generation most markedly increased in moderately and extremely hyper-tensive groups, less markedly in hypotensive group, but least seriously in normo-tensive group. It is coacluded that the blood pressure should be regulated to normal level (90-130mmHg) during precedure of reperfusion after the cerebral ischemia improves, to reduce the generation of free radicals and alleviate the brain damage.

本实验通过对45只兔血和脑组织中丙二醛(MDA)和超氧化物岐化酶(SOD)含量变化及组织病理改变的观测,探讨了脑缺血再灌流时不同水平血压对自由基脑损害的影响。结果提示,正常血压组动物的脑损害较轻,略低血压组次之,高血压及超高血压组脑损害较重。因此,于脑缺血后再灌流时,将血压控制在90~130mmHg范围内,有益于减轻自由基脑损害。

Using a modified method of Pulsinelli's induction of brain ischemic damage in wistar rat by 4-vessel occlusion, calcium content in hippocampus was found significantly higher in ischemic group. Nimodipine (1 mg/kg) was injected intraperitoneally following brain ischemia, the calcium content in hippocampus had no significant difference between Nimodipine treated group and ischemic group.

本文将51只雄性Wistar大鼠随机分成假手术对照组、缺血组、缺血-尼莫地平组。采用改良Pulsinelli法建立鼠脑缺血模型,并经脑电图监测及组织病理学检查证实缺血模型是成功的。缺血-尼莫地平组的大鼠在夹闭颈总动脉造成鼠脑暂时性缺血的同时於腹腔内注射尼莫地平。比较对照组及暂时性缺血再灌注72小时后海马组织钙含量,用原子吸收分光光度计测定发现缺血组海马组织钙含量增高,但缺血-尼莫地平组海马组织钙含量与缺血组差异无显著性。

According to hemodynamic principle,an animal model of cerebral ischemia-reperfu-sion injury was accomplished in rats applying method of carotid artery shunt in the study. Left carotid common artery was ligated .bloodletting performed from right carotid common artery and effluent blood transfused into femoral vein. Ischemic duration was 30,60,90 and 120 minutes respectively. Thereafter, ligation of left carotid common artery was released and bloodletting stopped. Observation lasted for 60 minutes during reperfusion....

According to hemodynamic principle,an animal model of cerebral ischemia-reperfu-sion injury was accomplished in rats applying method of carotid artery shunt in the study. Left carotid common artery was ligated .bloodletting performed from right carotid common artery and effluent blood transfused into femoral vein. Ischemic duration was 30,60,90 and 120 minutes respectively. Thereafter, ligation of left carotid common artery was released and bloodletting stopped. Observation lasted for 60 minutes during reperfusion. Throughout the experiment, the electroencephalographic activity,pupillary colour and mean artery blood pressure were monitored. The histological and ultrastructural changes were observed. The results indicated that electroencephalographic activity was suppressed severely during 15 minutes after cerebral ischemia and no recovery was observed during the remainder ischemic and following reperfusion duration. Pupillary colour was pale in Ischemia and bloody in reperfusion. Mean artery blood pressure was in normal range. The histological and ultrastrctural observation showed that with the more prolonged duration of ischemic,the more ischemic damage deteriorated and it would worsen further after reperfusion.

结扎大鼠左侧颈总动脉,从右侧颈总动脉远心端放血,放出的血液由股静脉输回体内,持续放血时间分别为30、60、90和120min;然后解除左侧颈总动脉结扎,同时停止放血,继续观察60min。动态观察脑电图、瞳孔颜色和动脉血压,进行光镜和电镜检查。结果发现在放血15min后,脑电波变平,以后未见恢复;随着缺血时间延长,缺血性损害相应加重,再灌后进一步恶化。

 
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