高氧致新生鼠急性肺损伤及氧化应激反应的动态研究

Dynamic study on acute injury and oxidative stress in lung of neonatal rats induced by hyperoxia

目的研究新生鼠暴露于高浓度氧不同时间后肺组织的病理改变,以及肺组织氧化应激反应状况。方法新生鼠暴露于>95%O2和正常空气(21%O2)中,取暴露12、24、48和72 h 4个时相点的肺组织,观察其病理变化,检测肺组织匀浆中丙二醛(malondiadehyde,MDA)含量、总抗氧化能力(total anti-oxygen capability,TAOC)。结果新生鼠暴露于>95%O212 h即可引起肺组织损伤,肺组织MDA含量显著升高(P<0.01),TAOC显著降低(P<0.01);随着氧暴露时间延长,MDA含量逐渐增高,TAOC逐渐降低,肺损伤加重,肺组织病理学检查可见肺组织微血管扩张、充血,肺泡内蛋白渗出,炎症细胞浸润,肺组织结构紊乱,肺大泡数量增多,II型肺泡上皮细胞脱落等。结论新生鼠暴露于>95%O212 h即可导致肺损伤和肺组织氧化应激反应的发生,高氧肺损伤与肺组织氧化应激反应有关。

Objective To study the pathologic alteration and oxidative stress in lung of neonatal rats exposed to hyperoxia for different time. Methods Neonatal rats less than 12 hours old were exposed to 〉 95%O2 and normal air（21%O2） respectively, and their lung were obtained when they had been exposed for 12, 24, 48 and 72 hours. The pathologic alteration in lung was observed by using light microscope and transmission electron microscope. The content of malondiadehyde（MDA） in lung homogenate was measured by Thiobarbituric Acid Test, and the total anti-oxygen capability （TAOC） was measured by Chemistry Colorimetry. Results Neonatal rats＇lung were injuryed after exposed to 〉95 % O2 for 12 hours, at the same time, the content of MDA increased significantly （ P 〈 0.01）, but the TAOC decreased significantly （ P 〈 0.01 ）. With the exposure time prolonging, the content of MDA increased, the TAOC decreased, and the lung injury was aggravated gradually. The pathologic alteration included microvessel hyperemia, inflammatory cell infiltration, hemorrhage, swollen endoplasmic reticulum and mitochondrion, and deciduous Ⅱ type alveolar epithelial cells. Conclusion Exposed to 〉95 % O2 for 12 hours can cause acute injury and oxidative stress in lung of neonatal rats. The longer the time is, the more severe the lung injury is, and there is relation between the lung injury and oxidative stress.