Brain Hypoxia

While the 134 mg / kg dose could also significantly promote the brain hypoxia tolerance , normal hypoxia tolerance and heat resistance abilities ( P < 0.01 or P < 0.05 ) .

炒紫苏子134mg/kg剂量组和溶媒15月龄小鼠阴性对照组比较，可显著提高耐脑缺氧能力、常压耐缺氧能力和耐高温能力（P<0.01或P<0.05）。

A Study of the Relationship between Acute Brain Hypoxia and Epilepsy in Rabbits

急性脑缺氧癫痫并发症的实验病理研究

We will discuss the role of NF - κ B for brain hypoxia - ischemia in this article .

本文主要探讨NF-κB在缺血缺氧性脑损伤中扮演的角色。

Effects of hypoxic pretreatment on changes in cerebral ultrastructure and free radical content induced by brain hypoxia and ischemia

缺氧预处理对缺血缺氧脑组织超微结构与自由基的影响

It was found that the occurrence of epilepsy was not in close relation with the severity of brain hypoxia .

结果表明癫痫的有无与脑缺氧的严重程度并不成正比。

Conclusion HBO increased both bFGF and bFGF mRNA expression of neonatal rats after brain hypoxia - ischemia injury .

结论HBO增强新生鼠缺血缺氧性脑损伤后bFGF及其mRNA表达。

In order to study the relationship between acute brain hypoxia and epilepsy , acute brain hypoxia was induced in 12 rabbits and the clinical manifestations were observed .

为观察急性脑缺氧与癫痫的关系，我们采用12只家兔造成急性脑缺氧的模型。

Objective : In order to get rid of children convulsion states quickly . Contact the time of brain hypoxia , to reduce damage of grain tissue and prevent relapse .

目的：使小儿尽快摆脱惊厥状态，缩短大脑缺氧时间，以减少脑实质损伤，并防止复发。

Conclusion Earlier HBO treatment can elevate the oxygen saturation in blood to block the malicious cycle of brain hypoxia , so as to increase the clinical cure rate and improve the living quality of the patients .

结论早期的HBO治疗可以及时提高血氧含量，阻止恶性缺血缺氧的发生。重症脑挫裂伤患者术后在可能的条件下应尽早行HBO治疗，以提高患者的生存质量。

Conclusions : Dynorphin A 1 ￣ 13 plays a role in the pathophysiological process of brain hypoxia ischemia and excessive amount of dynorphin A 1 ￣ 13 had some detrimental effect on the process .

结论：强啡肽A1～13参与脑缺氧、缺血的病理过程，过量的强啡肽A1～13有加重脑缺氧、缺血后病理改变的作用。

Changes and clinical significance of phosphodiesterase activity in rat brain during hypoxia

低氧大鼠脑组织磷酸二酯酶活性的变化及意义

Expression of Hypoxia Inducible Factor-1 in the Brain of Hypoxia Preconditioned Mouse

缺氧预适应小鼠脑组织中缺氧诱导因子-1的表达

Blood vase of lung brain with hypoxia have been contracted by the plasma dynorphin which have depressed respiratory action .

血浆强啡肽具有缺氧性肺脑血管收缩和抑制呼吸的作用。

Mild hypothermia therapy may reduce the brain tissue hypoxia and acidosis , and improve the prog ˉ nosis .

亚低温治疗能有效缓解SHI后的脑组织缺氧及酸中毒，从而改善患者预后。

The poor tolerance of brain to hypoxia is related to the high level of brain ATP , which is synthesized rapidly and utilized quickly within the brain .

脑对缺氧耐受性差与脑内ATP高稳定水平有关，即脑ATP迅速生成及迅速利用。

The results indicated that the mechanism of improving cerebral oxygen supply was carried out through improving the tolerance of important organs-heart and brain for hypoxia and antifatigue .

结果表明参七含片改善脑供氧作用机理是通过提高动物心脑等重要器官对缺氧的耐受力及对动物的机体有显著的抗疲劳作用实现的。

Effect of Glu on brain damage after hypoxia injury

谷氨酸在低氧性脑损伤中的作用

Conclusions BFGF can penetrate placental barrier , and protect brain cells from hypoxia and stimulate neurons proliferation .

结论bFGF能够通过胎盘屏障并促进宫内窘迫胎鼠神经元增殖并增加神经元存活数。

Objective The aim of this study was to investigate the role of diphenylhydantoin ( DPH ) in protection of brain against acute hypoxia .

目的探讨苯妥英钠（Diphenylhydantoin，DPH）在急性缺氧条件下的脑保护作用。

Even if patients make it to a hospital , permanent coma and even brain death from hypoxia may occur , given potentially long transport times to get medical care .

即使病人被送去医院，也可能会出现永久性昏迷，甚至可能出现大脑因缺氧死亡，因为要通过长时间的运输才能得到医疗护理。

Aim : To observe Nogo-A , Ng-R mRNA expression in the neonatal rat brain tissue after hypoxia ischemic brain damage ( HIBD ) .

目的：观察Nogo-A、Ng-rmRNA在缺氧缺血新生鼠损伤脑组织中表达量的变化。

Changes of Na ~ + , k ~ + - ATPase activity , lipid peroxides , lactic acid levels on brain damage during hypoxia under simulated plateau environment condition

模拟海拔8000米缺氧大鼠脑内钠钾ATP酶活性、脂质过氧化物和乳酸含量的变化

Conclusion At the early stage after CMW , there are obstructions to cerebral microcirculation , which induce brain ischemia , hypoxia and secondary failure of cerebral function .

结论CMW后早期出现微循环障碍，导致脑缺血缺氧，引起神经功能障碍；

TFP can also markedly inhibit the increase of the excitatory amino acid ( EAAS ) in the culture medium of brain slices during hypoxia ( P0.05 ) .

同时，TFP也可显著地抑制缺氧所致脑片孵育液中兴奋性氨基酸含量的增加（P0.05）。

Conclusion The expression of HIF 1 α is increased in brain on the hypoxia condition , which indicates that HIF 1 α may play an important role in the pathogenesis of hypoxic cerebral injury .

结论缺氧可诱导HIF-1α在大脑神经元中的表达。HIF-1α可能参与了缺氧性脑损伤过程。

Objective To determine the expression of inducible nitric oxide synthase ( iNOS ) in brain after cerebral hypoxia / reoxygenation and the effects of preoxygenation with different concentrations of oxygen in rats .

目的探讨缺氧复氧大鼠脑诱导型一氧化氮合酶（iNOS）的表达及预吸氧的效应。

Mitochondrial apoptotic signaling pathway in neurons following brain injury induced by hypoxia

脑缺氧损伤后线粒体途径神经元凋亡

Changes of adenylate pool and energy charge in mitochondria isolated from rat brain exposed to hypobaric hypoxia

低压缺氧大鼠脑线粒体内腺苷酸含量及能荷的变化

Conclusions Staying in constant magnetic field especially pole N possesses preventive effect against impairment of brain induced by acute hypoxia .

结论非均匀恒磁场对缺氧引起的障碍有预防性作用，可改善由缺氧造成的记忆功能损害，并减轻脑神经元的病理变化，N极作用更为明显。

Protective effects of plant of rehmannia root extract on mitochondrial respiratory function of heart , brain and kidney in hypoxia rat

地黄对缺氧大鼠心脑肾线粒体呼吸功能的保护作用