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采用大鼠油酸型呼吸窘迫综合征的病理模型（ｉｖ油酸０．１ｍＬｋｇ－１）．实验前２４ｈｉｐ眼镜蛇毒因子（ＣＶＦ）１．０ｍｇｋｇ－１耗竭体内补体，能显著对抗油酸引起的肺损伤：使支气管肺泡灌洗液中的细胞计数从（１５±１１）×１０１０Ｌ－１下降至（６±４）×１０１０Ｌ－１，蛋白质含量从５．２±１．９ｇＬ－１降至２．４±１．３ｇＬ－１；减少氧自由基的产生，血清超氧化物歧化酶活性下降和丙二醛含量升高明显受到抑制；降低溶酶体酶的释放，表现为血清β－葡萄糖醛酸酶活性降低；肺病理形态学的改变减轻，其中肺水肿程度，透明膜和肺动脉血栓形成均明显减轻．结果表明补体可能在油酸性肺损伤中起着重要作用，ＣＶＦ耗竭补体能显著减轻肺损伤．
A rat model of oleic acid-induced respiratory distress syndrome (iv oleic acid 0.1 mL kg-1) was used. Exhaustion of body complement in 24hip cobra venom factor (CVF) 1.0mgkg-1 significantly inhibited the oleic acid-induced lung injury before the experiment: the cell count in bronchoalveolar lavage fluid was decreased from (15 ± 11) × 1010L-1 to (6 ± 4) × 1010L-1, and the protein content decreased from 5.2 ± 1.9gL-1 to 2.4 ± 1.3gL-1, decreased the production of oxygen free radicals and decreased the activity of serum superoxide dismutase The increase of malondialdehyde was obviously inhibited; the release of lysosomal enzyme was reduced, the serum β-glucuronidase activity was decreased; the pathological changes of lung were alleviated, and the degree of pulmonary edema, hyaline membrane and pulmonary thrombosis Obviously relieved. The results suggest that complement may play an important role in oleic acid-induced lung injury, depletion of CVF can significantly reduce lung injury.