机械通气对小鼠肺损伤的初步研究

The study of ventilator induced lung injury in mice

目的建立小鼠机械通气肺损伤(VILI)模型,研究大潮气量、高浓度氧疗以及不同机械通气时间对VILI的影响及其可能机制。方法将C57BL/6雄性小鼠随机分为9组,对小鼠进行机械通气,再对小鼠进行支气管肺泡灌洗,采用双抗体夹心法检测肺泡灌洗液中总蛋白含量和炎症因子水平;小鼠肺组织石蜡包埋切片后行HE染色,显微镜下观察肺组织形态变化及损伤程度。结果大潮气量组小鼠肺泡灌洗液中总蛋白、炎症因子含量明显高于低潮气量组(P<0.05);高浓度氧疗组小鼠肺泡灌洗液中总蛋白、炎症因子含量明显高于低浓度氧疗组(P<0.05),并且随着通气时间的延长而升高;与正常对照组相比,各实验组小鼠肺泡灌洗液中蛋白含量明显升高(P<0.01);HE染色显示大潮气量机械通气4 h后,小鼠肺组织肺间隔明显增厚、炎性细胞浸润以及肺泡中出现渗出物,部分肺泡中出现红细胞的渗出等。结论大潮气量、高浓度氧疗均产生了明显的VILI,主要表现为肺组织急性炎症反应、渗透性肺水肿、氧化应激反应。

Objective To establish the model of ventilator-induced lung injury （ VILI） in mice, and to investigatetidal volume, high concentriation of oxygen therapy and different venlilation duralion on VILI. Methods C57BL/6 mice were randomly divided inlo nine groups according to the experimental designs for mechanical ventilation. At the end of lhe ventilation, the mice were sacrificed and the alveolar bronchial lavage fluid （BALV） from the mice was harvested. Then the lotal protein and inflammatory eytokines in the BALF were measured. Lung tissue change of the damage was observed by paraffin slice and HE staining in mice. Results Compared with the BAI,F of low- VT ventilated mice, higher total protein and inflammatory cylokines in the BA1,F were found in lhe group of high- VT. Total prolein in the BAI,F at 4 hours after mechanical ventilation were significantly higher than those of 2 hours ventilation. Cytokines in the BAI＋F were too low to be detected in the euntrol animals. In addition, with HE stai- ning, lung edema and inflammatory cells infihration were seen in the lung of mice after high tidal volume ventilation. Conclusion High-VT with hyperoxia can induce cytokine production, pulmonary edema, inflammatory cells infiltration. In addition, longer ventilation time may lead to more severe damage in the lung.