Gross N J, Smith D M
J Appl Physiol Respir Environ Exerc Physiol. 1981 Nov;51(5):1198-203. doi: 10.1152/jappl.1981.51.5.1198.
We studied the effect of 98% O2 on the amounts of and in vivo and in vitro synthesis rates of lung phospholipids in the mouse. The alveolar fluid obtained by multiple endobronchial lavages showed a decline in the amounts of all phospholipids between 48 and 72 h. The proportion of phosphatidylcholine that was disaturated did not change up to 96 h. Smaller decreases in phosphatidylcholine of the lung tissue were found at the same times. Between 48 and 72 h the turnover of total and disaturated phosphatidylcholine was greatly decreased, and transit time for both from lung to alveolar fluid was prolonged. At 60 h in vitro incorporation by lung slices of both glycerol and palmitate into disaturated phospholipids was reduced by approximately half, the distribution of label into various phospholipid classes being unchanged. We interpret these data as supporting the hypothesis that hyperoxia impairs the synthesis of surfactant phospholipids in the lung and their transport to the alveolar surface, and that this results in a decrease in the phospholipid content of the alveolar lining layer. These effects could account for altered pulmonary mechanical properties and contribute to the morbidity and mortality of O2 toxicity.
我们研究了98%氧气对小鼠肺磷脂体内外合成速率及含量的影响。通过多次支气管内灌洗获得的肺泡液显示，在48至72小时之间，所有磷脂的含量均下降。在96小时之前，双饱和磷脂酰胆碱的比例没有变化。同时发现肺组织中磷脂酰胆碱的减少幅度较小。在48至72小时之间，总磷脂酰胆碱和双饱和磷脂酰胆碱的周转率大幅下降，两者从肺到肺泡液的转运时间延长。在60小时时，肺切片将甘油和棕榈酸酯体外掺入双饱和磷脂的量减少了约一半，标记物在各种磷脂类别中的分布没有变化。我们认为这些数据支持以下假设：高氧会损害肺表面活性物质磷脂的合成及其向肺泡表面的转运，这会导致肺泡内衬层磷脂含量降低。这些影响可能解释肺机械性能的改变，并导致氧中毒的发病率和死亡率上升。
