Zenri Hiromi, Rodriquez-Capote Karina, McCaig Lynda, Yao Li-Juan, Brackenbury Angela, Possmayer Fred, Veldhuizen Ruud, Lewis Jim
Department of Medicine, Lawson Health Research Institute, St. Joseph's Health Centre, The University of Western Ontario, London, Ontario, Canada.
Crit Care Med. 2004 May;32(5):1155-60. doi: 10.1097/01.ccm.0000126264.00551.c8.
To evaluate the effects of hyperoxia exposure on lung function and the endogenous surfactant system in spontaneously breathing adult rats.
Analysis of the pulmonary surfactant system isolated from adult rats following exposure to > 90% oxygen or room air for 48 or 72 hrs.
A basic science research laboratory in a university setting.
Sixty pathogen-free Sprague-Dawley rats.
Exposure to > 90% oxygen for 72 hrs.
Exposure to > 90% oxygen for 72 hrs resulted in significant lung dysfunction and an increase in neutrophils and total protein concentrations within the airspace compared with animals exposed to room air or 48 hrs of 90% oxygen exposure. Total alveolar surfactant and large aggregate pool sizes were increased after 72 hrs of hyperoxia compared with the other groups, and there was evidence of lipid peroxidation within these large aggregate subtractions. The biophysical function of large aggregate isolated from 72-hr hyperoxia-exposed animals was also impaired and converted into small aggregate forms faster than large aggregate from normoxia-exposed animals when assessed using in vitro surface area cycling techniques.
Oxidative stress on the endogenous surfactant system may represent an important mechanism contributing to the surfactant dysfunction and abnormal surfactant metabolism associated with hyperoxia-induced lung injury.
评估高氧暴露对自主呼吸成年大鼠肺功能和内源性表面活性剂系统的影响。
对暴露于>90%氧气或室内空气48或72小时后的成年大鼠分离出的肺表面活性剂系统进行分析。
大学环境中的基础科学研究实验室。
60只无病原体的Sprague-Dawley大鼠。
暴露于>90%氧气72小时。
与暴露于室内空气或90%氧气48小时的动物相比,暴露于>90%氧气72小时导致明显的肺功能障碍,气腔内中性粒细胞和总蛋白浓度增加。与其他组相比,高氧暴露72小时后总肺泡表面活性剂和大聚集体池大小增加,并且在这些大聚集体部分中有脂质过氧化的证据。当使用体外表面积循环技术评估时,从暴露于72小时高氧的动物中分离出的大聚集体的生物物理功能也受损,并且比从暴露于常氧的动物中分离出的大聚集体更快地转化为小聚集体形式。
内源性表面活性剂系统上的氧化应激可能是导致与高氧诱导的肺损伤相关的表面活性剂功能障碍和异常表面活性剂代谢的重要机制。