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兴奋性氨基酸、ＮＭ ＤＡ 受体和一氧化氮合酶／一氧化氮系统参与了缺氧性脑损伤的形成，急性重复缺氧则能通过缺氧预适应显著提高小鼠对缺氧的耐受性。本研究旨在观察外源离子型ＮＭ ＤＡ 受体激动剂天门冬氨酸和抑制剂氯氨酮对小鼠缺氧预适应的形成以及形成过程中ＮＯＳ在小鼠海马脑区表达的影响。取昆明小鼠随机分为天冬氨酸、氯氨酸和正常对照三组，分别腹腔注射天门冬氨酸（３ ｇ／ｋｇ）、氯氨酮（１００ ｍ ｇ／ｋｇ）和生理盐水（３ ｍ ｌ／ｋｇ）；分别造成各组动物急性重复缺氧１ 次和４ 次同时测定各组缺氧耐受时间，并采用ＮＡＤＰＨｄ 组织化学技术观察各组动物脑内ＮＯＳ的表达。结果表明：天冬氨酸和氯氨酮分别显著地缩短和延长了小鼠的标准耐受时间。缺氧１ 次后，各组动物脑内ＮＯＳ的表达增强，而４ 次缺氧后，由于缺氧预适应的形成ＮＯＳ的表达未继续增加而保持不变。三组动物在缺氧４ 次后脑内ＮＯＳ的表达依次为天门冬氨酸组＞ 正常对照组＞ 氯氨酮组。上述结果提示：ＮＯＳ的抑制可能有益于缺氧耐受，并可能是预适应的机制之一。离子型ＮＭＤＡ 受体的激活和抑制分别不利于和有利于缺氧预适应的形成，这也可能是因为受体的激活和抑制分别促进和抑制了ＮＯＳ在海马的表达。
Excitatory amino acids, NMDA receptor and nitric oxide synthase / nitric oxide system are involved in the formation of hypoxic brain injury. Acute hypoxia can significantly increase hypoxic tolerance in mice through hypoxic preconditioning Sex. This study aimed to observe the effect of exogenous NMDA receptor agonist aspartate and ketamine on hypoxic preconditioning and the expression of NOS in the hippocampus of mice during the process of mouse hypoxia. The Kunming mice were randomly divided into three groups: aspartic acid, choline acid and normal control. The mice were injected intraperitoneally with aspartate (3 g / kg), ketamine (100 mg / kg) and normal saline (3 ml, respectively) .Acute hypoxia was repeated 1 and 4 times respectively in each group to determine the hypoxia tolerance time of each group. NADPH-d histochemical technique was used to observe the expression of NOS in each group. The results showed that aspartate and ketamine significantly shortened and prolonged the standard tolerated time in mice, respectively. After hypoxia for 1 time, the expression of NOS in each group of animals increased, but after 4 times of hypoxia, the expression of NOS did not increase due to hypoxia preconditioning. The expression of NOS in the three groups of animals after hypoxia four times in turn was aspartic acid group> normal control group> ketamine group. These results suggest that inhibition of NOS may be beneficial to hypoxia tolerance and may be one of the mechanisms of preconditioning. Ionic NMDA receptor activation and inhibition were not conducive to and conducive to the formation of hypoxic preconditioning, which may also be due to activation and inhibition of receptor respectively promote and inhibit the expression of NOS in the hippocampus.