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85%高浓度氧长期暴露诱发早产大鼠肺损伤(英文)
引用本文:钱莉玲,常立文,张谦慎,容志惠. 85%高浓度氧长期暴露诱发早产大鼠肺损伤(英文)[J]. 中国当代儿科杂志, 2003, 5(2): 95-99
作者姓名:钱莉玲  常立文  张谦慎  容志惠
作者单位:钱莉玲,常立文,张谦慎,容志惠
基金项目:Supported by the grant from Committe of Science and Technology of Hubei Province(No.2000ZP1601)
摘    要: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。

关 键 词:高浓度氧  肺损伤  早产  大鼠  

Lung Injury of Preterm Rats Induced by Prolonged Exposure to High Oxygen Concentration of 85%
QIAN Li-Ling,CHANG Li-Wen,ZHANG Qian-Shen,RONG Zhi-Hui. Lung Injury of Preterm Rats Induced by Prolonged Exposure to High Oxygen Concentration of 85%[J]. Chinese journal of contemporary pediatrics, 2003, 5(2): 95-99
Authors:QIAN Li-Ling  CHANG Li-Wen  ZHANG Qian-Shen  RONG Zhi-Hui
Affiliation:QIAN Li-Ling, CHANG Li-Wen, ZHANG Qian-Shen, RONG Zhi-Hui
Abstract:OBJECTIVE: To study the deleterious effect of prolonged hyperoxia exposure on preterm rat lungs. METHODS: On the 2nd postnatal day, preterm SD rats were randomly assigned to the air group (I) and hyperoxia group (II, exposed to 85% O2). After 3, 7 and 14 days of exposure, the contents of total protein (TP), hydroxyproline (HYP) and malondialdehyde (MDA), total cell counts and differentiation in bronchoalveolar lavage fluid (BALF), ratio of lung wet weight/dry weight (W/D), and lung collagen content were examined. After 3, 7, 14 and 21 days of exposure, lung histopathology and radial alveolar counts (RAC) were performed. RESULTS: On day 3 of hyperoxia exposure, only the MDA content increased in Group II(P<0.05). On day 7 and 14, TP, HYP, total cell counts, the percentage of neutrophils in BALF and lung W/D also significantly increased ( P < 0.05 or 0.01). The differences of lung collagen contents between the two groups were not significant ( P >0.05). Hyperoxia exposure resulted in subacute alveolitis and inhibition of lung development on day 7, 14 and 21. RAC was similar between the two groups on day 3 (4.9±0.7 vs 5.0 ±0.8), but different on day 7 (5. 9 ± 0.9 vs 7.1 ± 0. 9; P <0.05. On day 14 and 21, RAC decreased more obviously in Group II compared with that in Group I (7.0±0.8vs9.9±0.6, 7.3 ± 0.9vs10.5±0.8; P <0.01). CONCLUSIONS: Prolonged exposure to 85% O2 may result in subacute inflammatory lung injury and inhibition of lung development in preterm rats.
Keywords:Hyperoxia  Lung injury  Preterm  Rat
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