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目的通过观察不同间歇低氧(IH)模式下人脐静脉内皮细胞中内皮素-1(ET-1)浓度、一氧化氮(NO)浓度、一氧化氮合酶(NOS)活性及内皮型一氧化氮合酶(eNOS)mRNA 表达,探讨内皮功能障碍在阻塞性睡眠呼吸暂停综合征合并高血压发病机制中的作用。方法采用人脐静脉内皮细胞可传代细胞株 ECV304细胞系,暴露于不同的低氧/再氧合条件。暴露完成后测定 ET-1浓度(酶免疫测定,EIA)、一氧化氮浓度(硝酸还原酶法)、NOS 活性(化学比色法)及 eNOS mRNA 表达(RT-PCR)。结果间歇低氧组与间歇正常氧组及空白对照组比较,ET-1浓度升高(F=28.453,P=0.000),NO 浓度降低(F=65.252,P=0.000),NOS 活性(F=5.969,P=0.008)及 eNOS mRNA 表达下降(F=16.630,P=0.000)。相同累加低氧时间及程度的间歇低氧组与持续低氧组比较 ET-1浓度升高(t=2.742,P=0.024),NO 浓度降低(t=3.347,P=0.004),NOS 活性(t=3.989,P=0.004)及eNOS mRNA 表达下降(t=5.045,P=0.000);且不同频率间歇低氧组随再氧合时间的延长,ET-1浓度呈增加趋势(F=213.254,P=0.000),而 NO 浓度(F=15.747,P=0.000)、NOS 活性(F=2.933,P=0.048)及 eNOS mRNA 表达下降(F=5.954,P=0.002),但当再氧合时间过长时 ET-1浓度下降,NO 系统各指标上调。结论间歇低氧的低氧及再氧合过程均可导致内皮功能障碍、NO 和 ET-1释放失衡,从而促进了阻塞性睡眠呼吸暂停相关心血管疾病的发生和发展。
Objective To observe the effects of intermittent hypoxia (IH) on the levels of endothelin-1 (ET-1), nitric oxide (NO), nitric oxide synthase (NOS) Nitric oxide synthase (eNOS) mRNA expression, to explore the role of endothelial dysfunction in the pathogenesis of obstructive sleep apnea syndrome complicated with hypertension. Methods Human umbilical vein endothelial cells (ECV304) were transfected into ECV304 cell line and exposed to different hypoxia / reoxygenation conditions. ET-1 concentration (Enzyme immunoassay, EIA), nitric oxide concentration (nitrate reductase method), NOS activity (chemical colorimetry) and eNOS mRNA expression (RT-PCR) were determined after exposure was completed. Results Compared with intermittent normoxia group and intermittent normoxia group, the ET-1 concentration increased (F = 28.453, P = 0.000), NO decreased (F = 65.252, P = 0.000) 5.969, P = 0.008) and decreased eNOS mRNA expression (F = 16.630, P = 0.000). The concentration of ET-1 in the intermittent hypoxia group and the continuous hypoxia group were significantly higher than those in the continuous hypoxia group (t = 2.742, P = 0.024), NO concentration decreased (t = 3.347, P = 0.004) (t = 3.989, P = 0.004) and eNOS mRNA expression (t = 5.045, P = 0.000). The ET-1 concentration increased with the prolongation of reoxygenation time in intermittent hypoxia group (F = 213.254, (P = 0.000, P = 0.000). NO concentration (F = 15.747, P = 0.000), NOS activity (F = 2.933, P = 0.048) and eNOS mRNA expression decreased (F = 5.954, P = 0.002) Over long ET-1 concentration decreased, NO system indicators increased. Conclusions Intermittent hypoxic hypoxia and reoxygenation may result in endothelial dysfunction and the imbalance of NO and ET-1 release, thus promoting the occurrence and development of obstructive sleep apnea-related cardiovascular diseases.