Youssef J A, Thibeault D W, Rezaiekhaligh M H, Mabry S M, Norberg M I, Truog W E
University of Missouri-Kansas City and Children's Mercy Hospital, Kansas City, Mo., USA.
Biol Neonate. 1999 Mar;75(3):199-209. doi: 10.1159/000014096.
This study was undertaken to examine the combined effect of nitric oxide (NO) and hyperoxia on lung edema and Na,K-ATPase expression. Newborn piglets were exposed to room air (FiO2 = 0.21), room air plus 50 ppm NO, hyperoxia (FiO2 >/= 0.96) or to hyperoxia plus 50 ppm NO for 4-5 days. Animals exposed to NO in room air experienced only a slight decrease in Na,K-ATPase alpha subunit protein level. Hyperoxia, in the absence of NO, induced both the mRNA and the protein level of Na,K-ATP-ase alpha subunit and significantly increased wet lung weight, extravascular lung water, and alveolar permeability. NO in hyperoxia decreased the hyperoxic-mediated induction of Na,K-ATPase alpha subunit mRNA and protein while wet lung weight, extravascular lung water, and alveolar permeability remained elevated. These results suggest that 50 ppm of inhaled NO may not improve hyperoxic-induced lung injury and may interfere with the expression of Na,K-ATPase which constitutes a part of the cellular defense mechanism against oxygen toxicity.
本研究旨在探讨一氧化氮(NO)与高氧对肺水肿及钠钾ATP酶表达的联合作用。将新生仔猪暴露于室内空气(FiO2 = 0.21)、室内空气加50 ppm NO、高氧(FiO2 ≥ 0.96)或高氧加50 ppm NO环境中4 - 5天。暴露于室内空气中的NO的动物,其钠钾ATP酶α亚基蛋白水平仅略有下降。在无NO的情况下,高氧诱导了钠钾ATP酶α亚基的mRNA和蛋白水平,并显著增加了肺湿重、肺血管外水分及肺泡通透性。高氧环境中的NO降低了高氧介导的钠钾ATP酶α亚基mRNA和蛋白的诱导作用,而肺湿重、肺血管外水分及肺泡通透性仍保持升高。这些结果表明,吸入50 ppm的NO可能无法改善高氧诱导的肺损伤,且可能干扰钠钾ATP酶的表达,而该酶构成了细胞对抗氧毒性防御机制的一部分。