高浓度氧诱发急性肺损伤发病机制的探讨

Study on Mechanism of Hyperoxia-Induced Acute Lung Injury

目的:探讨高浓度氧造成急性肺损伤的发生机制。方法:将雄性6周龄Wistar鼠30只分为对照组(空气中饲养,n=20)和实验组(暴露在90%～95%氧气中72h,n=10)。结果:实验组动物外周血中的红细胞(RBC)、血红蛋白(Hb)及红细胞比容(HCT)计数高于对照组(P<0.05);实验组动物外周血RBC、Hb计数随高浓度氧暴露时间的延长逐渐升高;对照组中动物体质量持续增长,而实验组动物体质量首日轻度增加,第2天开始呈现逐渐下降的趋势;对照组气管肺泡清洗液(BALF)中以巨噬细胞为主,而实验组BALF中可见大量中性粒细胞浸润;实验组动物均出现双侧胸水。结论:中性粒细胞动员并进入肺组织是高浓度氧诱发急性肺损伤的明显特征;营养不良可能是诱发急性肺损伤的因素之一,早期抑制中性粒细胞进入肺组织和纠正营养不良是治疗高浓度氧诱发急性肺损伤的重要途径。

Objective： To explore the mechanism of acute lung injury （ALI） caused by high concentration oxygen exposure. Methods： Thirty young male Wistar rats were divided into two groups which included control group （exposed to room air, n=20） and experimental group （exposed to 90%-95% oxygen for 72 h, n =10）. Results： The level of RBC, Hb and HCT in blood in experimental group was higher than those in control group. RBC and Hb in blood increased gradually with the duration of high concentration oxygen exposure in experimental group. The body weight of the rats in control group increased. The body weight of rats in experimental group increased slightly at the first day and lose from the second day. The cell influx into hronchoalveolar lavage fluid （BALF） was macrophage in control group, and neutrophil in the experimental group. All rats were noted to have bilateral pleural effusions in experimental group. Conclusions： An increase of neutrophil count is an evident feature of hyperoxia-induced lung injury and high concentration oxygen exposure can give rise to anorexia and malnutrition which may play a role in hyperoxia-induced lung injury. Blocking neutrophil influx into lung tissue in the early phase and improving malnutrition are two effective methods in reducing hyperoxic lung injury.