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- acute hypoxic exposure 急性低氧暴露
- But in chronic hypoxic exposure, the inhibition of both RNA synthesis and protein synthesis was alleviated, being 72% and 76% of the normoxic control, respectively. 慢性缺氧暴露后线粒体RNA和蛋白质合成活性分别为对照的72%25和76%25;
- Fig 2 4 weeks hypoxic exposure, the cardio-fibra cells edema, mitochondria swollen and interstitium edema occurred.The empty bulb of mitochondria increased. 2缺氧4周，心肌感冒细胞水肿，线粒体肿胀，空泡增多。
- Objective To study the effect of acute hypoxia and hypoxic acclimatization on myocardial function of rats. 目的研究低氧习服对大鼠心肌功能的影响。
- Effects of Acute Hypoxia on Plasma Lactic Acid and Lactic Dehydrogenase Content in Pilots. 急性低压缺氧对飞行人员血浆乳酸及乳酸脱氢酶含量的影响。
- Acute hypoxia induced a series of impairments in skeletal muscle mitochondrial bioenergetics. 急性低氧导致线粒体一系列生物能学功能障碍。
- The chromatograms of heart homogenate after acute hypoxia in mice were determine d by HPLC. 对小鼠进行急性重复性缺氧,并测定未缺氧小鼠及缺氧小鼠心脏匀浆高效液相色谱图。
- In this Review,we summarize the current knowledge regarding the effects of hypoxia on diaphragmatic fatigue,its mechanisms,and acclimatized alteration of diaphragm after hypoxic exposure. 对低氧造成膈肌疲劳的机制和机体对低氧后的适应性改变进行简要的介绍。
- AIM Protective action of TMP on hearts and brains under the condition of the acute hypoxia was studied. 目的对急性缺氧状态下川芎嗪(TMP)的保护作用进行探讨。
- CONCLUSION TMP has a notable protection on brains and hearts under the condition of acute hypoxia in mice. 结论TMP在急性缺氧状态下对心脑具有保护作用。
- Objective To explore the changes of blood brain barrier(BBB) permeability following acute altitude hypoxia exposures in rats. 目的 观察急性中、重度低压缺氧条件下 ,大鼠血脑屏障通透性的变化特点 ,为阐明低压缺氧作用下脑功能障碍的可能机理提供生理学依据。
- The results of the study suggest that proper IHH can protect developing rat heart against ischemia/reperfusion injury while this effect could be affected by mode of intermittent hypoxia exposure. 结果表明, 适当的IHH增强发育大鼠心脏对缺血/再灌注损伤的抵抗能力；间歇性低氧方式是影响间歇性低氧心脏保护作用的重要因素。
- 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。
- AIM: To explore the mechanism of ET-1, NO and PGI 2 release from coronary artery endothelial cells (CAEC) induced by acute hypoxia. 目的 :探讨低氧引起冠状动脉内皮细胞 (CAEC)释放ET - 1、NO和PGI2 改变的机制。
- METHODS:Male Sprague-Dawley(SD) rats were randomly divided into three groups: normoxia group(n=10),acute hypoxia group(n=10) and intermittent hypoxic group(n =10). 方法:SD雄性大鼠分为常氧组、急性低氧组和间歇低氧组,每组10只。
- METHODS: The mean survival time and capacity for myocardial oxygen consumption were detected in rats with acute hypoxia under ordinary or low pressure. 方法:常压和低压缺氧条件下分别观察小鼠平均存活时间和心肌耗氧量。
- Methods cAMP,PLA 2,Evans blue (EB) and water content of the brain tissue (WCB) were measured in rat after combined soman and acute hypoxia injury with microtitration and RIA. 方法 应用微量滴定、放免法从动物整体水平观察了高原缺氧、梭曼中毒单一与复合致伤后 1 2、2 4、48h大鼠脑组织含水率 (WCB)、伊文思蓝 (EB)含量、PLA2 的活性、环磷酸腺苷(cAMP)含量的变化。
- Hou ZH,Yu B,Wang ZZ.Effect of acute hypoxia alone and hypoxia combining exercise on skeletal muscle and activity of metabolizing enzymes.Chin J Clin Rehabil,2004,8:902-903. [2]侯振海;余斌;汪志忠.;急性低氧及低氧复合运动对骨骼肌及代谢酶活性的影响
- Conclusion These results suggest that acute hypoxia can strengthen the expression of HSP70 in guinea pig’s cochlea, and the degree of hypoxia has no effects on the degree of this strengthening. 结论急性缺氧可以诱导豚鼠耳蜗HSP70表达增强,表达部位与正常耳蜗组织相同,不同程度的缺氧对其表达的强度没有影响。
- I threatened him with public exposure. 我威胁说要向公众揭发他。
