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作者报告山羊内毒素肺损伤后有关的肺反应和动脉血、静脉血及肺淋巴引流液中脂质过氧化反应产物丙二醛(MDA)含量的改变,探讨氧自由基在内毒素肺损伤中的作用。结果:有关的肺反应指标符合内毒素肺损伤特点,主动脉血中MDA在内毒素致伤后1h和2h,分别由致伤前2.11±0.4nmol/ml增高至4.03±1.2和3.73±1.0nmol/ml(P<0.01),肺淋巴液中MDA致伤前为1.68±0.58nmol/ml,致伤后1h增加至2.94±0.67nmol/ml,2h达高峰为3.56±0.86nmol/ml,(P均<0.01);中心静脉血中MDA无显著增高。提示脂质过氧化反应在内毒素肺损伤及ARDS形成中超重要作用;动脉血中MDA增高而静脉血中不增高时可能反映有内毒素所致肺损伤存在。
The authors report changes in lung response and arterial blood, venous blood, and the lipid peroxidation product malondialdehyde (MDA) content in the lung lymphatic drainage fluid following endotoxin-induced lung injury in goats to investigate the role of oxygen free radicals in endotoxin-induced lung injury Role. Results: The lung function indicators were consistent with the characteristics of endotoxin-induced lung injury. MDA in aorta blood increased from 2.11 ± 0.4 nmol / ml to 4.03 ± 1.2 and 3.73 ± 1.0 nmol at 1 h and 2 h after injury / ml (P <0.01), MDA in lung lymph was 1.68 ± 0.58nmol / ml before injury and increased to 2.94 ± 0.67nmol / ml at 1h after injury, reaching 3.56 ± 0.86nmol / ml at 2h All <0.01); central venous blood MDA was not significantly increased. These results suggest that lipid peroxidation plays an important role in the pathogenesis of endotoxin-induced lung injury and ARDS. The increase of MDA in arterial blood and the non-increase of venous blood may reflect the existence of endotoxin-induced lung injury.