Storme L, Zerimech F, Riou Y, Martin-Ponthieu A, Devisme L, Slomianny C, Klosowski S, Dewailly E, Cneude F, Zandecki M, Dupuis B, Lequien P
Department of Neonatology, CHRU de Lille, France.
Biol Neonate. 1998;73(3):172-81. doi: 10.1159/000013975.
The purpose of this investigation was to examine whether inhaled nitric oxide (NO) may alter oxidative stress parameters and induce lung inflammation in moderate hyaline membrane disease (HMD). Eighteen moderately premature lambs (130 days gestation, term = 147 days) were randomly assigned to treatment with 20 ppm inhaled NO (n = 8) from the onset of ventilation or used as control (n = 10). Except inhaled NO, treatments were intentionally similar to those applied in clinical situations. The main studied parameters were oxidative stress index measurements on lung parenchyma and in circulating blood, lung parenchyma microscopic examination and bronchoalveolar lavage cell count. We found that 20 ppm of inhaled NO for 5 h did not change significantly either malondialdehyde and total antioxidant status levels in circulating blood, or malondialdehyde, reduced glutathione, glutathione peroxidase and glutathione reductase in lung parenchyma. Amino-imino-propene bond generation, which are lipoperoxidation markers, was similar in both groups. Furthermore, no significant changes in the number of inflammatory cells in lung lavage products and in lung parenchyma microscopic examination could be found. Therefore, these data do not support the hypothesis that short-term NO inhalation increases oxidative stress and lung inflammation in an experimental model of moderate HMD.
本研究的目的是探讨吸入一氧化氮(NO)是否会改变中度透明膜病(HMD)中的氧化应激参数并引发肺部炎症。18只中度早产羔羊(妊娠130天,足月为147天)从通气开始时被随机分配接受20 ppm吸入NO治疗(n = 8)或用作对照(n = 10)。除吸入NO外,治疗方法有意与临床情况中应用的方法相似。主要研究参数包括肺实质和循环血液中的氧化应激指数测量、肺实质显微镜检查以及支气管肺泡灌洗细胞计数。我们发现,吸入20 ppm NO 5小时后,循环血液中的丙二醛和总抗氧化状态水平,以及肺实质中的丙二醛、还原型谷胱甘肽、谷胱甘肽过氧化物酶和谷胱甘肽还原酶均无显著变化。两组中作为脂质过氧化标志物的氨基 - 亚氨基丙烯键生成情况相似。此外,在肺灌洗产物中的炎性细胞数量以及肺实质显微镜检查中均未发现显著变化。因此,这些数据不支持在中度HMD实验模型中短期吸入NO会增加氧化应激和肺部炎症这一假设。