目的：观察高原ＲＤＳ时ＳＰ－Ａ、ＳＰ－Ｂ和ＳＰ－ＣｍＲＮＡ表达与影响因素，了解其变化情况，并探讨其在急性肺损伤中的作用机制及意义。方法：采用高原ＲＤＳ动物模型，利用分子生物学技术观察肺组织肺泡Ⅱ型上皮细胞表面活性蛋白及其基因的表达。结果：ＳＰ－Ａ、ＳＰ－Ｂ和ＳＰ－Ｃ斑点杂交结果表明，油酸组ＳＰ－Ａ，ＳＰ－Ｂ和ＳＰ－ＣｍＲＮＡ表达的相对含量均显著低于对照组。油酸可抑制ＳＰ－Ａ，ＳＰ－Ｂ和ＳＰ－ＣｍＲＮＡ在高原ＲＤＳ中的表达。结论：高原ＲＤＳ后ＳＰ－Ａ、ＳＰ－Ｂ和ＳＰ－ＣｍＲＮＡ表达明显减低，油酸可抑制ＳＰ－Ａ，ＳＰ－Ｂ和ＳＰ－ＣｍＲＮＡ在高原ＲＤＳ中的表达。与油酸的直接毒性作用和油酸引起的肺水肿，肺泡腔渗出大量的水肿液及血浆蛋白有关 OBJECTIVE: To observe the expression and influencing factors of SP-A, SP-B and SP-CmRNA in the plateau RDS and to understand their changes, and to explore its mechanism and significance in acute lung injury. Methods: Using plateau RDS animal model, the expression of surfactant protein and its gene in alveolar type Ⅱ epithelial cells in lung tissues was observed by molecular biology techniques. Results: The SP-A, SP-B and SP-C spots hybridization results showed that the relative content of SP-A, SP-B and SP-CmRNA in oleic acid group were significantly lower than the control group. Oleic acid inhibits the expression of SP-A, SP-B and SP-CmRNA in plateau RDS. CONCLUSIONS: The expressions of SP-A, SP-B and SP-CmRNA were significantly decreased after plateau RDS. Oleic acid inhibited the expression of SP-A, SP-B and SP-CmRNA in plateau RDS. The direct toxicity with oleic acid and oleic acid-induced pulmonary edema, alveolar exudate a lot of edema fluid and plasma proteins