一氧化氮吸入对急性高浓度氧肺损伤新生大鼠肺水通道蛋白1和5表达的影响

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48 h；（2）高浓度氧组(O)：予高浓度氧持续吸入48 h，维持FiO₂＞0.95；(3)高浓度氧+NO组(ONO)：予高浓度氧持续吸入48 h，维持FiO₂＞0．95，前24 h同时予1×10-5NO吸入；（4）空气 + NO组(CN)： 予空气48 h，前24 h同时予1×10^-5NO吸入。各组分别测肺组织湿重/干重比值(Q_W/Q_D)，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AQP1 mRNA含量明显低于正常对照组(0.68±0.38 vs 1.81±0.76， P<0.01)，AQP5mRNA含量无明显变化。1×10^-5 NO+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AQP1 mRNA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24 h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。

Effect of inhaled nitric oxide on aquaporin expression in newborn rat lung in acute hyperoxic lung injury

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 (Q_W/Q_D), the histology, and AQP1, AQP5, α₁-NKA, α-ENaC mRNA expressions in the lungs were measured. RESULTS:Compared with C group, the Q_W/Q_D 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 Q_W/Q_D (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 hyperoxic 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.