高浓度氧对新生大鼠肺氧自由基损伤及其发育的影响

The Effect of Prolonged Hyperoxia on Neonatal Rat Lung

【目的】观察持续吸入高浓度氧后新生大鼠发育中肺的病理及肺组织内脂质过氧化物的变化,探讨高浓度氧对新生大鼠肺发育的影响。【方法】新生大鼠出生后分别在90%以上氧和空气中持续暴露,于d3、d7、d14、d21,动态观察肺组织病理学改变和胶原染色面积的变化以及肺组织8-异前列腺素F2α含量。【结果】与空气对照组比较,高氧组肺泡发育受阻,出现肺泡变大且结构简单化、肺泡数目减少等肺泡发育不良的慢性肺疾病病理表现,肺损伤逐渐加重,最终纤维化;胶原染色阳性面积于d7时高于对照组,随时间延长而逐渐增加;8-异前列腺素F2α含量d3时升高,d7时最高,以后下降但至d21仍高于对照。【结论】高氧对新生大鼠肺有明显损害,使其肺发育受阻,最终出现胶原增加的纤维化改变;氧化损伤可能是引起慢性高氧肺损伤的原因之一。

[Objective]To observe the change of lung histology and oxidative stress reaction in neonatal rat exposed to hyperoxia, to determine the effect of prolonged hyperoxia on the development of neonatal rat lung. [Methods]The full-term newborn rats were randomly assigned into a hyperoxia group（ HO group） and a Control group（Con group）. The HO group was continuously given a high concentration of oxygen （FiO2〉 0.90） and the Con group received oxygen with the FiO2 of 0.21 after birth. The lung histological change, collagen area and the concentration of the 8-isoprostane2α, a specific marker for in vivo lipid peroxidation,in lung were monitered on day 3,7,14 and 21 in two groups. [Results]Compared with the Con group , the arrest of lung development was accompanied by interstitial fibrosis and increased collagen deposition, which was evident after 7d of oxygen exposure, increasing through 21d, resembled to the histology of chronic lung disease（CLD） which appeared as fewer and bigger alveoli. The level of 8-isoprostane2α increased at 3d and reached peak at 7d, then decreased, but still remained at a higher level on the 21st day than that of the Con group. [Conclusion]Prolonged hyperoxia exposure appears to lead to an arrest of lung development. The lung oxidative stress reaction is closely related to the hyperoxia -induced lung injury.