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目的：为了解急性缺氧后大鼠肾组织一氧化氮合酶（ＮＯＳ） 基因表达的变化，探讨急性缺氧引起肾损害的分子机制。方法：１５ 只雄性Ｗｉｓｔａｒ 大鼠随机分成对照、缺氧后１０ ｍｉｎ 组、缺氧４ ｈ 组。实验组大鼠在低压舱内模拟上升至５０００ ｍ 、停留４５ ｍｉｎ 、出舱后分别在１０ ｍｉｎ 、４ ｈ 处死大鼠取肾，提取总ＲＮＡ，用反转录聚合酶链反应（ＲＴＰＣＲ） 定量检测大鼠肾组织内ｂＮＯＳｍ ＲＮＡ、ｅＮＯＳｍ ＲＮＡ、ｉＮＯＳｍ ＲＮＡ 的表达水平。结果：ｂＮＯＳ 在急性缺氧后１０ｍｉｎ 明显下降，４ ｈ 后恢复正常；ｅＮＯＳ 急性缺氧后１０ ｍｉｎ 、４ ｈ 无明显变化；ｉＮＯＳ 急性缺氧后１０ ｍｉｎ 无变化，至４ ｈ则无基因表达。结论：急性缺氧可导致大鼠ｂＮＯＳ、ｉＮＯＳ 表达下调，ＮＯ 可能参与了急性缺氧所致的肾组织及整体的病理生理过程，但有可能是可逆的。
AIM: To investigate the changes of gene expression of nitric oxide synthase (NOS) in rat kidney after acute hypoxia and explore the molecular mechanism of acute hypoxia-induced renal damage. Methods: Fifteen male Wistar rats were randomly divided into control group, 10 min hypoxia group and 4 h hypoxia group. Rats in the experimental group were raised to 5000 m in low pressure cabin and stayed for 45 min. Rats were sacrificed after 10 min and 4 h, respectively. The total RNA was extracted and the total RNA was extracted by reverse transcription-polymerase chain reaction ) Quantitative detection of bNOSm RNA, eNOSm RNA, iNOSm RNA expression in rat renal tissue. Results: The bNOS decreased significantly 10 min after acute hypoxia and returned to normal after 4 h. There was no significant change at 10 min and 4 h after eNOS acute hypoxia. No change was observed 10 min after iNOS acute hypoxia and no gene expression was observed at 4 h. CONCLUSION: Acute hypoxia can lead to the down-regulation of bNOS and iNOS expression in rats. NO may be involved in renal tissue and the whole pathophysiological process induced by acute hypoxia, but it may be reversible.