目的：SP-A在维持肺表面活性物质（PS）功能和肺局部免疫功能方面起着重要作用。该文旨在探讨急性肺损伤（ALI）时肺组织SP-A随时间的变化规律。方法：无病原体的21日龄Sprague-Dawley幼鼠110只被随机分为正常对照组和ALI组（每组又分为6个亚组）。腹腔注射脂多糖（LPS，4 mg/kg）建立ALI模型，正常对照组注射等量生理盐水。LPS注射后6，12，24，36，48和72 h每亚组各处死8只大鼠。 用Western blot方法测定肺组织SP-A的相对含量。结果：与正常对照组相比，ALI时肺组织SP-A的变化在12 h内无明显变化(P＞ 0.05)； 在24 h 至48 h处于上升阶段（P＜ 0.01）， 于36 h达最高点（6.94±0.80）；到72 h时SP-A下降(P＜0.01)。结论：肺组织SP-A在LPS诱导的ALI中的变化为时间依赖性。肺组织SP-A一过性升高，表现出SP-A在某种程度上的代偿能力较强。

OBJECTIVE: Pulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury. METHODS: Sprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues. RESULTS: SP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94±0.80 vs 5.01±0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01). CONCLUSIONS: The changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.