Nitric oxide attenuates lung endothelial injury caused by sublethal hyperoxia in rats.
Nitric oxide attenuates lung endothelial injury caused by sublethal hyperoxia in rats.
复制标题
一氧化氮减轻大鼠亚致死高氧引起的肺内皮损伤。
DOI：
10.1152/ajplung.1997.272.4.l631
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Pittet,JF
中科院分区：
文献类型：
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作者：
McElroy,MC;Wiener-Kronish,JP;Miyazaki,H;Sawa,T;Modelska,K;Dobbs,LG;Pittet,JF
吸入一氧化氮（NO）已被证明可以防止氧化剂诱导的肺损伤隔离灌注肺模型，而NO衍生的氧化剂可能有助于继发于高氧的急性肺损伤。吸入NO是否改善或有助于氧化剂介导的肺损伤可能取决于NO给药的时机或如何评估肺损伤。这些研究的目的是确定是否吸入NO（20 ppm）是保护性的或有害的不同的肺屏障时，它与95%的O2在Sprague-Dawley大鼠60小时，通过测量液体运输和蛋白质的渗透性肺内皮细胞和肺泡上皮细胞。吸入NO显着减弱O2介导的肺内皮损伤，并取消了支气管肺泡灌洗液中rTI 40含量的增加，rTI 40是肺泡上皮I型细胞损伤的特异性和敏感性标志物，继发于高氧。总之，吸入NO与高浓度的O2给药可以保护肺内皮细胞和肺泡上皮细胞免受O2介导的损伤。
Inhaled nitric oxide (NO) has been shown to prevent oxidant-induced lung injury in isolated-perfused lung models, whereas NO-derived oxidants may contribute to acute lung injury secondary to hyperoxia. Whether inhaled NO improves or contributes to oxidant-mediated lung injury may depend on the timing of NO administration or how lung injury is assessed. The objective of these studies was to determine whether inhaled NO (20 ppm) was protective or harmful to the different lung barriers when it was administered with 95% O2 for 60 h in Sprague-Dawley rats by measuring fluid transport and permeability to protein across the lung endothelium and the alveolar epithelium. Inhaled NO significantly attenuated the O2-mediated lung endothelial injury and abolished the increase in the bronchoalveolar lavage fluid content of rTI40, a specific and sensitive marker of alveolar epithelial type I cell injury, that occurs secondary to hyperoxia. In conclusion, inhaled NO administered with high concentrations of O2 may protect the lung endothelium and the alveolar epithelium against O2-mediated injury.