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目的探讨模拟高空环境、间歇性缺氧暴露（６ｈ／ｄ×６ｄ）条件下，大鼠脑皮质兴奋性氨基酸（ｅｘｃｉｔａｔｏｒｙａｍｉｎｏａｃｉｄ，ＥＡＡ）含量变化、神经细胞内Ｃａ２＋含量、脑皮质超微结构改变以及应用ＮＭＤＡ受体拮抗剂后ＥＥＡ及细胞内Ｃａ２＋含量的变化。方法选择４８只健康Ｗｉｓｔａｒ大鼠，雌雄不限，随机分成６组，采用梯度洗脱方式分离氨基酸，用ＯＰＡ柱前衍生法、高效液相色谱柱（ＯＤＳＣ１８）分离，荧光检测组织细胞氨基酸含量，荧光探针测定皮质细胞内Ｃａ２＋含量。结果模拟高空缺氧环境可使ＥＡＡ释放增加，从而导致突触后ＥＡＡ受体过度被刺激，产生离子依赖性兴奋毒。随着缺氧程度加大，在一定范围内细胞内ＥＡＡ的释放随之增加，胞内钙离子浓度上升，变化较明显，神经细胞内线粒体、内质网水肿，有空泡出现，胞浆稀疏，ＮＭＤＡ受体拮抗剂氯胺酮对ＥＡＡ的释放有一定的抑制作用，细胞内Ｃａ２＋浓度增加趋缓。其中６ｋｍ、８ｋｍ高度Ｇｌｕ、Ａｓｐ含量与对照组比，有非常显著性差异（Ｐ＜０．０１）。细胞内Ｃａ２＋浓度的增加与对照组比，有非常显著性差异（Ｐ＜０．０１）。结论缺氧、尤其严重缺氧可导致ＥＡＡ的大量释放，ＥＡＡ释放的增加是Ｃａ２＋内流的重要因素?
Objective To investigate the changes of excitatory aminoacid (EAA) content, intracellular Ca2 + content and ultrastructure of cerebral cortex under simulated high altitude and intermittent hypoxia exposure (6h / d × 6d) Changes of EEA and intracellular Ca2 + after NMDA receptor antagonist. Methods Forty - eight healthy Wistar rats were randomly divided into 6 groups. The amino acids were separated by gradient elution. The amino acids were separated by OPA pre column derivatization and high performance liquid chromatography (ODSC18) Fluorescence probe to detect intracellular Ca2 + content. Results Simulating the hypoxic environment at high altitude could increase the release of EAA, leading to excessive stimulation of post-synaptic EAA receptors and generation of ion-dependent excitotoxicity. With the increase of hypoxia, within a certain range of intracellular EAA release increased, intracellular calcium concentration increased, the change was more obvious, nerve cells mitochondria, endoplasmic reticulum edema, vacuoles, cytoplasmic sparse Ketamine, an NMDA receptor antagonist, inhibited the release of EAA, and the increase of intracellular Ca2 + concentration was slowed down. The Glu and Asp concentrations at 6km and 8km were significantly different from those in the control group (P <0.01). There was a significant difference between the increase of intracellular Ca2 + concentration and the control group (P <0.01). Conclusion Hypoxia, especially severe hypoxia, can lead to the massive release of EAA. The increase of EAA release is an important factor of Ca2 + influx.