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ischemic brain injury
相关语句
  缺血性脑损伤
    DYNAMIC CHANGES OF LEVELS OF VASOACTIVE INTESTINAL PEPTIDE AND SUBSTANCE P IN PLASMA AFTER HYPOXIC ISCHEMIC BRAIN INJURY IN NEONATAL RATS
    新生大鼠缺氧缺血性脑损伤后血浆血管活性肠肽和P物质水平的动态变化
短句来源
    Dynamic changes in levels of vasoactive intestinal peptide and adrenocorticotropic hormone in the brain after hypoxic ischemic brain injury
    新生大鼠缺氧缺血性脑损伤后脑内血管活性肠肽和促肾上腺皮质激素的动态变化
短句来源
    Possible Mechanism of Electroacupuncture Preconditioning for Hypoxia/Ischemic Brain Injury Protection Effect in Neonatal Rats
    电针预处理对新生大鼠缺氧缺血性脑损伤保护作用的可能机制
短句来源
    Protective effects of activin on the neurons of neonatal rats with hypoxic ischemic brain injury
    激活素对新生大鼠缺氧缺血性脑损伤后神经元的保护
短句来源
    The Change of Insulin-like Growth Factor-1 and the Affection on Neurogenesis after Ischemic Brain Injury
    胰岛素样生长因子-1在缺氧缺血性脑损伤后的变化及对神经生成的影响
短句来源
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  血性脑损伤
    DYNAMIC CHANGES OF LEVELS OF VASOACTIVE INTESTINAL PEPTIDE AND SUBSTANCE P IN PLASMA AFTER HYPOXIC ISCHEMIC BRAIN INJURY IN NEONATAL RATS
    新生大鼠缺氧缺血性脑损伤后血浆血管活性肠肽和P物质水平的动态变化
短句来源
    Dynamic changes in levels of vasoactive intestinal peptide and adrenocorticotropic hormone in the brain after hypoxic ischemic brain injury
    新生大鼠缺氧缺血性脑损伤后脑内血管活性肠肽和促肾上腺皮质激素的动态变化
短句来源
    Possible Mechanism of Electroacupuncture Preconditioning for Hypoxia/Ischemic Brain Injury Protection Effect in Neonatal Rats
    电针预处理对新生大鼠缺氧缺血性脑损伤保护作用的可能机制
短句来源
    Protective effects of activin on the neurons of neonatal rats with hypoxic ischemic brain injury
    激活素对新生大鼠缺氧缺血性脑损伤后神经元的保护
短句来源
    The Change of Insulin-like Growth Factor-1 and the Affection on Neurogenesis after Ischemic Brain Injury
    胰岛素样生长因子-1在缺氧缺血性脑损伤后的变化及对神经生成的影响
短句来源
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  “ischemic brain injury”译为未确定词的双语例句
    N-acetylcysteine (NAC) has been reported to have antioxidant and anti-inflammation effects which attenuate ischemic brain injury in adult animal models. There was no report concerning NAC on neonatal brain injury.
    N-乙酰半胱氨酸(NAC,N-acetylcysteine)具有抗氧化和抗炎症的作用,在成年脑缺氧缺血动物模型上有神经保护作用,对未成熟脑损伤的保护作用尚未见详细报道。
短句来源
    NOS inhibitor L NAME may make microcirculation dysfunction worse and lead to a further hypoxic ischemic brain injury.
    此时抑制内源性 NO的合成 ,可加重脑组织的微循环障碍而导致脑缺氧缺血性损害的进一步加重
短句来源
    Conclusions HI could induced the changes of the second messengers PKC and IP 3. The continuous PKC down regulation and c fos gene expression may take part in neuron injuries during hypoxic ischemic brain injury.
    结论 HIE诱导第二信使PKC及IP
短句来源
    Conclusion: Present data suggest that dynorphinA 1-13 contributes to the pathophysiological changes of hypoxic ischemic brain injury not only via opiate-receptor mediated but probably a combination of nonopioid mechanisms.
    结论 :强啡肽A1-13 对新生鼠缺氧、缺血脑损伤的影响 ,除通过阿片途径外 ,尚可能通过其它非阿片途径共同作用而实现的。
短句来源
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  ischemic brain injury
Inhibition of neurotransmitter release may, in part, be responsible for the protective effect of pentobarbital in ischemic brain injury.
      
This study demonstrated that bradykinin postconditioning induces protection against ischemic brain injury and promotes neuronal survival.
      
Plasticity of Neurons and Glia Following Neonatal Hypoxic-Ischemic Brain Injury in Rats
      
We propose the monitoring of serine, asparagine, and threonine, together with excitatory amino acids, as an index of the degree of ischemic brain injury.
      
Research on ischemic brain injury has established a central role of mitochondria in neuron death (1-3).
      
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bjective To determine the effect of high risk obstetric factors on neonatal hypoxic-ischemic brain injuries. The obstetric factors were investlgated,including maternal complications during pregnancy and labor,the mcde of delivery. Methods Intensive B-ultrasound brain monitoring in 211 newborns within the first 48 hours of life was carried out.The abnormalities were followed up by B-ultrasound.We assessed the extent of hypo- xic-ischemic brain injuries with two kind of types,mild and severe....

bjective To determine the effect of high risk obstetric factors on neonatal hypoxic-ischemic brain injuries. The obstetric factors were investlgated,including maternal complications during pregnancy and labor,the mcde of delivery. Methods Intensive B-ultrasound brain monitoring in 211 newborns within the first 48 hours of life was carried out.The abnormalities were followed up by B-ultrasound.We assessed the extent of hypo- xic-ischemic brain injuries with two kind of types,mild and severe. The mild type included 1-2 degree intracranial hemorrhage and the local hypoxic-ischemic encephalopathy. The severe type included 3-4 degree intracranial hemorrhage and extensive cerebral edema. Results Thirty-nine cases(18. 5%)were diagnosed intracranial hemorrhage and 22 cases(10.4%)vvere diagnosed hypoxic-ischemic encephalopathy(HIE)or cerebral edema. The total positive rate was 28.9%。Of the positive cases,67.2%were mild brain injuries without clinical symptoms. Those cases need no medical treatment and recovered in a natural course. The rates of brain injuries in groups of pregnancy induced hypertension,fetal distress, neonatal asphyxia and premature newborns,were 46.1%,48.9%,66.7%and 71.4%respectively.It suggested that high risk obstetric factors were closely related to neonatal brain injuries. 15.9%of positive cases were from normal mothers with- out any obstetric complications. The brain injuries in those cases were mild.Conclusions The study showed that as a non-invasive procedure,B ultrasound brain examination is necessary for newborns with perinatal high risk factors of brain injuries. The study also suggested that perinatal care and systematic fetal monitoring were key-points for reduction of neonatal brain injuries.

为从母亲孕期、产时合并症及分娩方式等方面探讨引起新生儿缺氧性脑损伤的高危因素,对211例新生儿于出生后48小时内进行颅脑8超检查。结果:新生儿颅内出血39例(18.5%),脑缺氧缺血改变、脑水肿22例(10.4%),总阳性率28.9%。其中轻型脑损伤67.2%,无临床症状,不需处理即可自行恢复。母亲好高征患儿、胎儿宫内窘迫、新生儿窒息及早产儿的颅脑8超阳性率依次为46.1%、48.9%、66.7%和71.4%。围产期无任何合并症的新生儿颅脑B超阳性的仍有15.9%,但脑损伤程度较轻。提示:好高征、胎儿窘迫及早产系缺氧性脑损伤的主要高危因素,脑损伤程度较重。对有围产期高危因素的新生儿行颅脑B超的筛查是必要的。

Dynamic observation in measument of A Ⅱ ET and ALD in 35 cases of neonatal asphyxia and respiratory failure were reported. 20 cases of normal newborns were tested as controlled group. The results showed A Ⅱ value in acute stage was obviously higher than the convalesed stage (546. 80± 334. 52: 286. 44±278.0 ng/L)and also higher than the normal controlled group (384. 99±311. 13 ng/L) (P<0. 01). The increasement of A Ⅱ activity was related to the degree of hypoxia. The value of ET in acute stage was also higher...

Dynamic observation in measument of A Ⅱ ET and ALD in 35 cases of neonatal asphyxia and respiratory failure were reported. 20 cases of normal newborns were tested as controlled group. The results showed A Ⅱ value in acute stage was obviously higher than the convalesed stage (546. 80± 334. 52: 286. 44±278.0 ng/L)and also higher than the normal controlled group (384. 99±311. 13 ng/L) (P<0. 01). The increasement of A Ⅱ activity was related to the degree of hypoxia. The value of ET in acute stage was also higher that the convalesed stage and the normal controlled group. The value of ALD in acute stage was the highest htan all other group. Thus, For increasement of cerebral blood flow to improve hypoxic-ischemic brain injury to use vasodilatation durgs, early derection of A Ⅱ ET and ALD was suggested during asphyxia and respiratory failure.

本文报告了新生儿窒息呼吸衰竭35例血浆血管紧张素Ⅱ(AⅡ)、内皮素(ET)及醛固酮(ALD)的动态变化,20例正常新生儿作为对照组。结果显示:AⅡ急性期值明显高于缓解期(546.80±334.52:286.44±278.0ng/L)也高于正常新生儿对照组(384.99±311.13ng/L),P<0.01。随着缺氧程度加重AⅡ活性增高,ET急性期值也高于缓解期和正常对照组,而且急性期ALD明显高于其它组。因此,我们建议在窒息和呼吸衰竭时早期检测AⅡ、ET及ALD为使用血管扩张药以增加脑血流改善缺氧缺血脑损害提供依据。

AIM To explore the role of nitric oxide (NO) and endothelin (ET) in the early phase of hypoxic brain injuries by examing the effect of N ω nitro L arginine methyl ester (L NAME), an inhibitor of nitric oxide synthase (NOS), on brain NO production and serum ET level in newborn rats with hypoxic brain injuries. METHODS The rats were divided into normal control group, hypoxia group and L NAME+ hypoxia group. The ET level in serum, NO production, NOS activity, pathology and capillary perfusion in brain...

AIM To explore the role of nitric oxide (NO) and endothelin (ET) in the early phase of hypoxic brain injuries by examing the effect of N ω nitro L arginine methyl ester (L NAME), an inhibitor of nitric oxide synthase (NOS), on brain NO production and serum ET level in newborn rats with hypoxic brain injuries. METHODS The rats were divided into normal control group, hypoxia group and L NAME+ hypoxia group. The ET level in serum, NO production, NOS activity, pathology and capillary perfusion in brain were investigated in 3 groups. RESULTS The serum ET level of hypoxia group was significantly higher than that of controls ( P <0.01), but NO production and NOS activity were not significantly different between 2 groups ( P >0.05), and the brain capillary perfusion was more serious in hypoxia group that that in controls. Compared with the hypoxia group, the serum ET level of L NAME+ hypoxia group was increased significantly ( P <0.05), NO production and NOS activity in brain was decreased significantly ( P <0.01), and brain capillary perfusion was serious significantly ( P < 0.05 ). CONCLUSION Abnormal increase of serum ET in early phase of acute hypoxia is the main factor of brain injury; NOS inhibitor L NAME may make microcirculation dysfunction worse and lead to a further hypoxic ischemic brain injury.

目的 用新生大鼠急性缺氧模型 ,探讨 NO合成酶抑制剂 L-硝基 -精氨酸甲酯 (L- NAME)在缺氧后脑损伤中的作用 ,进而探讨一氧化氮 (NO)和内皮素 (ET)在早期缺氧性脑损伤中的作用地位 .方法 检测正常对照组、缺氧组和缺氧前应用 L- NAME预处理的新生大鼠血浆 ET及脑组织匀浆 NO含量及 NOS的活性 ,并观察各组大鼠脑组织病理改变及毛细血管充盈不良程度 .结果 缺氧组血浆 ET水平较正常对照组显著升高 (P<0 .0 1) ,而脑 NO水平及 NOS活性无显著变化 (P>0 .0 5 ) ,脑毛细血管充盈不良程度与正常对照组相比明显加重 (P<0 .0 5 ) ;L- NAME组血浆 ET水平较缺氧组显著升高 (P<0 .0 5 ) ,脑 NO含量及 NOS活性较缺氧组显著下降 (P<0 .0 1) ,脑毛细血管充盈不良程度与缺氧组相比明显加重 (P<0 .0 5 ) .结论 急性缺氧早期 ,ET异常增高是脑损伤的主要因素 ;此时抑制内源性 NO的合成 ,可加重脑组织的微循环障碍而导致脑缺氧缺血性损害的进一步加重

 
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