睡眠呼吸暂停低通气综合症的一部分——慢性间歇性低氧（CIH）被认为会对肺组织造成损害，而谷氨酸的作用尚未得到良好研究。我们使用了一种慢性长期间歇性低气压低氧（CLTIHH）大鼠模型，以确定此类程序是否会导致肺损伤以及N-甲基-D-天门冬氨酸受体的潜在影响（NMDARs），并使用受体拮抗剂MK-801（二唑西平）。 32只大鼠分为四组；一组对照组和三个CLTIHH组，其中大鼠被放置在低压室中，设定为430毫米汞柱，每天5小时，每周5天，持续5周。只有一组每天接受MK-801（0.3mg / kg，ip）治疗。 我们评估了炎症过程的肿瘤坏死因子（TNF）-α，白细胞介素（IL）-6，IL-10和核因子（NF）-kB，评估氧化应激的超氧物歧化酶（SOD），丙二醛（MDA），过氧化氢酶（CAT），谷胱甘肽过氧化酶（GPX），总抗氧化状态（TAS）和总氧化状态（TOS），以及caspase-9水平。评估了血浆，支气管肺泡灌洗液（BALF）和肺组织提取物。所有CLTIHH组介质中的氧化剂和炎症参数均明显增加，仅接受MK-801处理的组未增加。收集了MK-801减轻CLTIHH影响的有力证据。组织学评估显示CLTIHH组中的肺损伤和纤维化变化。首先证明了CLTIHH程序导致慢性肺损伤，并且炎症和氧化应激对肺损伤的形成有影响。其次，NMDAR拮抗剂MK-801有效抑制了肺损伤和纤维化的发展。

Chronic intermittent hypoxia (CIH), a component of sleep apnea-hypopnea syndrome, is suggested to cause damage to lung tissue, and the role of glutamate is not well studied. We used a chronic long-term intermittent hypobaric hypoxia (CLTIHH) model of rats to find out if such procedure causes lung injury and the potential effect of N-methyl-D-aspartate receptors (NMDARs) by using receptor antagonist MK-801 (dizocilpine). Thirty-two rats were placed into four groups; a control and three CLTIHH groups where rats were placed into a low-pressure chamber set to 430 mmHg for 5 h/day, 5 days/week, for 5 weeks. Only one group received MK-801 (0.3 mg/kg, ip) daily. We evaluated tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, and nuclear factor (NF)-kB for the inflammatory process, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), glutathione peroxidase (GPX), total antioxidant status (TAS), and total oxidant status (TOS) for oxidative stress, and caspase-9 levels. Blood plasma, bronchoalveolar fluid (BALF), and lung tissue extracts were evaluated. Both oxidant and inflammatory parameters were significantly increased in all the mediums of the CLTIHH groups except the group that received MK-801. Significant evidence was collected on MK-801 alleviating the effect of CLTIHH. Histological evaluations revealed lung damage and fibrotic changes in the CLTIHH groups. It was first shown that the CLTIHH procedure caused chronic lung injury, and that inflammation and oxidant stress were influential in the formation of lung injury. Secondly, NMDAR antagonist MK-801 effectively inhibited the development of lung injury and fibrosis.