肺泡中肺表面活性蛋白A反映冲击伤复合缺氧的肺损伤程度

The changes of pulmonary suffactant associated protein A in BALF with lung injury in rats with blast injury and blast injury combined with hypoxia

目的研究冲击伤及冲击伤复合缺氧时支气管肺泡灌洗液（BALF）中肺表面活性蛋白A（SP-A）含量变化与肺损伤的关系及意义。方法Wistar大鼠131只（野战外科研究所实验动物中心提供），随机分为4组：冲击伤（BI）组47只，冲击伤复合缺氧Ⅰ组（BAⅠ）36只，冲击伤复合缺氧Ⅱ组（BAⅡ）4JD只，正常对照（NC）组8只。用BST-Ⅰ型生物激波管致冲击伤，BAⅠ、BAⅡ组伤后立即置入低氧舱内，分别通入含12．5％和10％的O2的混合气体，并分别保持舱内氧的体积分数稳定在12．5％和10％。NC组大鼠不做任何处理。动物分别于伤后1、3、6h活杀，行大体解剖、光镜和电镜病理观察、肺含水量测定，Western blot法测定BALF中SP-A含量。计量资料数据以均数±标准差（x±s）表示，采用组间比较q检验和相关分析；计数资料采用χ^2检验。结果大鼠冲击伤后呼吸加快，BAⅠ组和BAⅡ组有烦躁不安、呼吸急促，BAⅡ组可见明显口鼻发绀；致伤各组肺含水率明显高于正常大鼠（P〈0．05）。肺大体解剖主要表现为肺出血、肺水肿，光镜下见肺泡壁增厚、肺泡腔出血、间质水肿；电镜下可见肺泡壁断裂，Ⅱ型上皮细胞板层体减少；这些改变均以BAⅡ组最重、BAⅠ次之、BI再次，6h的死亡率分别为37．5％、11．1％和2．1％（P〈0．01）。伤后BALF中SP-A浓度显著降低（P〈0．01），并与肺含水率呈显著负相关（r=-0．796，P〈0．01）。结论冲击伤复合缺氧显著加重肺部的损伤，缺氧越重、时间越长，则肺损伤越重、死亡率越高；BALF中SP-A含量的显著减少与肺水肿程度有关，BALF中SP-A含量可作为判断冲击伤及其复合伤肺损伤严重程度的观察指标。

Objective To investigate the changes of surfactant associated protein A （SP-A） concentration in BALF and its relationships with pulmonary injury after blast injury and blast injury combined with hypoxia. Method Totally 131 Wistar rats （purchased from animal center of research Institute of Surgery, Daping Hospital, Third Military Medical University） were randomly divided into four groups： blast injury group （BI group）, blast injury combined with hypoxia group Ⅰ （BA Ⅰ group）, blast injury combined with hypoxia group Ⅱ （BA Ⅱ group） and normal control group. After blast injury was made by BST- Ⅰ bio-shock tube, rats of BA Ⅰ and BA Ⅱ groups were put into hypoxia cabius immediately, where gas mixtures of 12.5% and 10.0% oxygeon were given, respectively. Rats were sacrificed at 1, 3 and 6 hours after injury for gross anatomic examination, light and electron microscope observation and lung water determination. The level of SP-A in BALF was detected by Western blot. The data were processed by t test or Chi-square test. Results The respiration increased with shortness of breath and dysphoria in rats of BA Ⅰ and BA Ⅱ groups,and obvious cyanosis on the lips and nose in rats of BA Ⅱ group after blast injury. The lung water in rats of all injury groups was significantly higher than that in normal control group （ P 〈 0.05 ）.Gross anatomy changes were mainly pulmonary bleeding and edema. Under light microscope, inerassation of alveolar wall, bleeding in alveolar and mesenchyme edema were found. Whereas under electron microscope, breakage of alveolar wall and decrease of lamellar bodies in type Ⅱ cell were observed. All these changes were most obvious in BAⅡ group followed by BAⅠ and BⅠ groups in severity decling order, with mortality rate of 37.5%, 11.1% and 2.1% respectively at 6 hours （ P 〈 0.01 ）. The SP-A level in BALF decreased significantly （ P 〈 0.01 ） and had a good negative relationship with the lung water after injury （ r = 0. 796, P 〈 0. 001 ）. Conclusions Blast injury combined with hypoxia significantly deteriorates the lung injury. More severe and longer hypoxia may result in more severe lung injury and higher mortality rate. A decrease in SP-A value in BALF shows a good negative relationship with the pulmonary edema. The SP-A can be a good indicator for lung injury severity after blast injury and blast injury combined with hypoxia.