大鼠支气管肺泡灌洗液内HSP70水平与肺损伤关系

Relationship of lung injury and heat shock protein(HSP70) within bronchial lavage fluid in rats

目的探讨不同潮气量机械通气后大鼠支气管肺泡灌洗液(BALF)内热休克蛋白(HSP70)和肺损伤的关系。方法健康SD大鼠36只,随机均分为3组:大潮气量机械通气组(HV)、小潮气量机械通气组(LV)、正常对照组(N)。采用ELISA法测定大鼠BALF中总蛋白质浓度、HSP70和白细胞介素6(IL-6)、巨噬细胞炎性蛋白2(MIP-2)的含量。结果①与N组比较,LV、HV组大鼠BALF中HSP70、IL-6、MIP-2水平以及肺损伤病理评分均升高(P<0.05);②与LV组比较,HV组大鼠BALF中HSP70、IL-6、MIP-2的水平和肺损伤病理评分显著升高(P<0.05);③HV组大鼠BALF中IL-6、MIP-2以及肺损伤病理评分别与HSP70呈正相关(r=0.853 8,P<0.05;r=0.891 9,P<0.05;r=0.885 2,P<0.05)。结论大潮气量机械通气可致肺上皮细胞损伤或坏死增加,HSP70胞外释放增加,肺内炎症反应显著增加;而小潮气量机械通气致肺组织损伤程度轻,细胞坏死少,HSP70胞外释放少;因此肺内炎症反应较大潮气量通气小。

Objective To explore the relationship of heat shock protein （HSP70） and lung injury under different tidal volume mechanical ventilation on rats. Methods 36 healthy male SD rats were randomly divided into three groups, according to different tidal volume as high tidal volume ventilation with room air inhalation （HV） , low tid- al volume ventilation with room air inhalation （LV） and room air inhalation without mechanical ventilation（N）. The adapted ELISA was used to determine the concentrations of total protein, HSP70, interlukin （IL-6）, macro- phage inflammatory protein （MIP-2） in bronchial lavage fluid （BALF） from the rats. Results The level of HSP70, IL-6 and MIP-2 in BALF from rats under low or high tidal volume ventilation increased significantly compared with that from rats of control group（ each P 〈 0. 05 ）. The same trend of lung injury score was seen within the above 3 experimental animals. Worthy to note that the concentrations of IL-6, MIP-2 and HSP70 from HV ventilated rats were significantly higher than those from LV ventilated rats （ each P 〈 0.05 ）, so did the lung injury score. In addi- tion, positive correlations were seen between HSP70 level in BALF and lung injury score from HV ventilated rats（ r = 0. 885 2, P 〈 0.05）. HSP70 also had positive correlation with concentration of IL-6 and MIP-2 in BALF （ r = 0. 853 8, P 〈 0. 05; r = 0. 891 9, P 〈 0. 05 respectively）. Conclusion Severe lung injury caused by high tidal volume ventilation could lead to increased airway epithelial cell injury or necrosis which resulted in the release of HSP70 from epithelial cells to the airway space and thus enhanced the inflammation of the lung.