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目的探讨长期高浓度氧(85％)暴露对早产新生大鼠肺组织的损伤作用。方法早产SD大鼠生后第2天被随机分为Ⅰ空气组、Ⅱ高氧组(置85％O2中)。分别于暴露3,7,14 d后,检测支气管肺泡灌洗液(BALF)中总蛋白(TP)、丙二醛(MDA)、羟脯氨酸(HYP)含量和细胞总数及分类,肺组织湿重/干重(W/D),肺组织胶原含量;于暴露3,7,14,21 d后,行肺组织病理学检查和辐射状肺泡计数(RAC)。结果3 d时Ⅱ组仅MDA含量增加(P<0.05);7,14 d时,Ⅱ组BALF中MDA,TP,HYP含量、细胞总数、细胞分类中性粒细胞所占比例及肺W/D均明显增加(P<0.05或<0.01)。两组肺胶原含量差异无显著性(P>0.05)。除3 d外,Ⅱ组肺组织病理学检查可见不同程度的肺泡炎改变和肺发育滞后。7 d时Ⅱ组RAC值较Ⅰ组明显减少[(5.9±0.9)vs(7.1±0.9)](P<0.05);14,21 d时RAC值Ⅱ组较Ⅰ组[(7.0±0.8)vs(9.9±0.6);(7.3±0.9)vs(10.5±0.8)]减少更明显(P<0.01)。结论85％O2长期暴露,可引起早产新生大鼠亚急性炎症性肺损伤和肺发育受抑。
Objective To investigate the effect of long-term high concentration oxygen (85%) exposure on lung injury in premature neonatal rats. Methods Sprague - Dawley rats were randomly divided into Ⅰ air group and Ⅱ hyperoxia group (85% O2) on the second day after birth. The levels of total protein (TP), malondialdehyde (MDA), hydroxyproline (HYP) and the total number of cells in bronchoalveolar lavage fluid (BALF) Wet weight / dry weight (W / D) and lung tissue collagen content. Lung histopathology and radial alveolar count (RAC) were performed at 3, 7, 14 and 21 days after exposure. Results At 3 d, only the content of MDA in group Ⅱ increased (P <0.05). At 7 and 14 d, the contents of MDA, TP and HYP in BALF, the total number of cells, the percentage of neutrophils in BALF and the ratio of lung W / D Were significantly increased (P <0.05 or <0.01). There was no significant difference in lung collagen content between the two groups (P> 0.05). Except for 3 days, the histopathological examination in group Ⅱ showed varying degrees of alveolitis and delayed lung development. (P <0.05). The RAC value of group Ⅱ was significantly lower than that of group Ⅰ [(5.9 ± 0.9) vs (7.1 ± 0.9) (9.9 ± 0.6); (7.3 ± 0.9) vs (10.5 ± 0.8)], respectively (P <0.01). Conclusion Long-term exposure of 85% O2 can cause subacute inflammatory lung injury and suppression of lung development in preterm born neonatal rats.