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本文观察了脂质过氧化在犬(n=16)烟雾吸入性肺损伤机制中的作用。测定了动脉血SOD活性、动脉血浆MDA及呼出气乙烷和PaO_2及EVLW的变化。结果表明,本模型伤后早期出现了肺水肿和急性肺功能障碍。MDA及乙烷伤后显著增加,伤后30min及24h出现两峰值,SOD活性办增加。提示伤后早期氧自由基增加,肺脂质过氧化亢进。MDA及乙烷的第一个峰值与早期肺损伤及应激反应有关,第二个峰值与肺部感染有关。MDA、乙烷及SOD活性变化规律与PaO_2及EVLW相同。表明氧自由基导致的脂质过氧化可能参与了烟雾吸入伤后肺损伤发生和发展。
This article investigates the role of lipid peroxidation in the mechanism of smoke-induced lung injury in dogs (n = 16). The changes of arterial blood SOD activity, arterial plasma MDA, exhaled ethane, PaO 2 and EVLW were measured. The results showed that pulmonary edema and acute pulmonary dysfunction occurred early after injury in this model. MDA and ethane injury increased significantly, 30min and 24h after injury showed two peaks, SOD activity increased. Prompted oxygen free radicals increased early injury, pulmonary lipid peroxidation. The first peak of MDA and ethane is associated with early lung injury and stress response, and the second peak is associated with lung infection. The changes of MDA, ethane and SOD activity were the same as PaO_2 and EVLW. It is suggested that lipid peroxidation induced by oxygen free radicals may be involved in the occurrence and development of lung injury after smoke inhalation injury.