Dodd K T, Gross D R
Arch Environ Health. 1980 Jan-Feb;35(1):6-14.
Twenty healthy conditioned cats were pulmonary-function tested and then exposed to 1000 ppm of ammonia gas for a 10-min period. Pulmonary function tests were repeated and lung samples for pathologic evaluation were taken on days 1, 7, 21, and 35 post-exposure. Two cats were housed with the experimental cats as untreated controls. Pulmonary function data were analyzed, statistically evaluated, and compared with the pathological observations. There was good correlation between the alterations in pulmonary function observed and the pathologic lesions found. According to our findings, and those of other investigators, the pulmonary dysfunction which results from ammonia gas inhalation is biphasic in nature. The acute effects of the initial insult, which can be fatal, are almost always followed by secondary effects which can result in debilitating, chronic respiratory dysfunction. This study has characterized an animal model which could provide techniques for preventing or modifying the course of the secondary damage of ammonia gas inhalation.
对20只健康的经训练的猫进行肺功能测试，然后使其暴露于1000 ppm的氨气中10分钟。重复进行肺功能测试，并在暴露后的第1、7、21和35天采集肺样本进行病理评估。将两只猫与实验猫一起饲养作为未处理的对照。对肺功能数据进行分析、统计评估，并与病理观察结果进行比较。观察到的肺功能改变与发现的病理病变之间存在良好的相关性。根据我们的研究结果以及其他研究者的结果，吸入氨气导致的肺功能障碍本质上是双相的。最初损伤的急性效应可能是致命的，几乎总是继之以继发效应，这可能导致使人虚弱的慢性呼吸功能障碍。本研究已对一种动物模型进行了表征，该模型可为预防或改变吸入氨气继发损伤的病程提供技术。
