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目的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大鼠随机分成对照组、缺氧后１０ｍｉｎ组、缺氧后４ｈ组。实验组大鼠在低压舱内模拟上升至５０００ｍ、停留４５ｍｉｎ，出舱后分别在１０ｍｉｎ、４ｈ处死大鼠取肾，提取总ＲＮＡ，用反转录聚合酶链反应（ＲＴ－ＰＣＲ）定量检测大鼠肾组织内ｂＮＯＳｍＲＮＡ、ｅＮＯＳｍＲＮＡ、ｉＮＯＳｍＲＮＡ的表达水平。结果ｂＮＯＳｍＲＮＡ在急性缺氧后１０ｍｉｎ明显下降，４ｈ后恢复正常；ｅＮＯＳｍＲＮＡ急性缺氧后１０ｍｉｎ、４ｈ无明显变化；ｉＮＯＳｍＲＮＡ急性缺氧后１０ｍｉｎ无变化，至４ｈ则无基因表达。结论急性缺氧可导致大鼠ｂＮＯＳｍＲＮＡ、ｉＮＯＳｍＲＮＡ表达下调，ＮＯ在急性缺氧的病理生理过程中起到重要作用。
Objective 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 experimental group were raised to 5000m in low pressure cabin for 45min, and then were sacrificed at 10min and 4h after release. Total RNA was extracted and quantitatively detected by reverse transcriptase-polymerase chain reaction (RT-PCR) The expression of bNOS mRNA, eNOS mRNA and iNOS mRNA in rat kidney tissue. Results The bNOS mRNA 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 acute hypoxia, but no change at 10 min after acute hypoxia and no gene expression at 4 h. Conclusion Acute hypoxia can lead to the down-regulation of bNOSmRNA and iNOSmRNA in rats, and NO plays an important role in the pathophysiology of acute hypoxia.