中文摘要：

目的：观察一氧化氮（NO）吸入对急性高浓度氧肺损伤新生大鼠肺上皮水转运体系的影响。方法：32只新生SD大鼠，随机分为：（1）空气组（C）：予空气48h；（2）高浓度氧组（O）：予高浓度氧持续吸入48h，维持FiO2〉0．95；（3）高浓度氧＋NO组（ONO）：予高浓度氧持续吸入48h，维持FiO2〉0．95，前24h同时予1×10^-5 NO吸入；（4）空气＋NO组（CN）：予空气48h，前24h同时予1×10^-5NO吸入。各组分别测肺组织湿重／干重比值（Q。／Q。），行肺组织病理学检查，用RT-PCR方法测定肺组织AQP1、AQP5、α1-NKA和α—ENaC mRNA含量。结果：高浓度氧组肺湿重／干重比值明显高于正常对照组（5．81±1．01 vs 4．33±0．94，P〈0．01）；而肺组织AQP1mRNA含量明显低于正常对照组（0．68±0．38 vs 1．81±0．76，P〈0．01），AQP5 mRNA含量无明显变化。1×10^-5NO＋高浓度氧组肺组织湿重／干重比值明显高于高浓度氧组（4．89±0．68 vs 5．81±1．01，P〈0．05）；而肺组织AQP1mRNA含量明显高于高浓度氧组（1．27±0．54 vs 0．68±0．38，P〈0．05），AQP5mRNA含量无明显变化。结论：1×10^-5NO吸入24h能减轻急性高浓度氧肺损伤新生大鼠的肺水肿，提高肺内水通道蛋白1mRNA含量，水通道蛋白5的mRNA含量无明显改变，提示1×10^-5NO的吸入可能对急性高浓度氧肺损伤新生大鼠肺内水通道蛋白1有一定的保护作用。

英文摘要：

AIM ： To investigate the effect of inhaled nitric oxide on aquaporin expression and alveolar epithelial fluid transport in newborn rats with acute hyperoxic lung injury. METHODS： 32 newborn SD rats were randomized to breathe for 48 h room air （ C）, 〉95% O2 （ O）, 〉95% O2 ＋ 10^-5 NO （ NO only in the first 24 h, ONO）, room air ＋ NO （CN）. Then, the rats were killed, the lung wet - to - dry weight ratio （ QW/QD ）, the histology, and AQP1, AQP5, α1 - NKA, α- ENaC mRNA expressions in the lungs were measured. RESULTS： Compared with C group, the Qw/QD in O group significantly increased （ P 〈 0. 01 ）, and AQP1 mRNA expression decreased significantly （ P 〈 0. 01 ）. Compared with O group, ONO group had a lower level of Qw/QD（ P 〈 0. 05） , and AQP1 mRNA expression increased （P 〈0. 05 ）. AQP5 mRNA expression in all groups remained unchanged. CONCLUSION： In newborn rats with acute hyperoxie lung injury, inhaled 10 ^-5 nitric oxide for 24 h may attenuate lung edema and increase AQP1 mRNA expression, suggesting that inhaled 10^-5 nitric oxide for 24 h may promote the AQP1 expression in lung in this model of acute lung injury.