脂质过氧化在烟雾吸入性肺损伤机制中的作用

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。

The Role of Lipid Peroxidation in Lung Damage after Smoke Inhalation

The role of lipid peroxidation in the precipitation of umg damage after smoke inhalation was investigated in 16 dogs. Superoxide dismutase(SOD) activity and plasma MDA in arterial blood, and ethane in the exhaled air were determined to demonstrate oxygen free radicals and lipid peroxidation. PaO2 and extravascular lung water (EVLW) were determined to evaluate lung damage.It was found that in the early postinjury period, the experimental animals suffered from pulmonary edema and acute pulmonary dysfunction. MDA in arterial plasma and exhaled ethane markedly increased (P<0.01) and reached two peaks 30 minuts and 24 hours postinjury. Meanwhile SOD activity in arterial blood also increased markedly. These facts imply that increase of oxygen free radicals and excessive lipid peroxidation exist in the lungs of the dogs. It is believed that the first peak of MDA and ethane is related to the onset of pulmonary damage and the stress response, and their second peak to the development of pulmonary infection. The patterns of MDA, ethane and SOD activity changes were similar to those of PaCO2 and EVLW, which implies that the excessive lipid peroxidation resulting from the increase of oxygen free radicals might participate in the onset and development of lung damage after smoke inhalation.