Currie W D, Pratt P C, Frosolono M F
Toxicol Ind Health. 1985 Oct;1(2):17-27. doi: 10.1177/074823378500100203.
Rats were exposed to phosgene at a concentration of 1.0 ppm for 4 hours in a Rochester-type chamber. At intervals thereafter over a 4 day period, lungs were obtained for histological and biochemical assessments. Edema was estimated by histological examination and by measurement of lung wet and dry weights. In parallel studies, pulmonary mitochondrial respiratory activity was measured using Clark oxygen electrodes. The significant reduction in respiratory control index (State 3 respiration/State 4 respiration) found immediately following phosgene exposure coincided with the highest level of % lung water. There was a concomitant decrease of ATP concentration that persisted on the third day after exposure. Na-K-ATPase activity was reduced 1 day after exposure, thus a lowered ATP level preceded a reduction in Na-K-ATPase or sodium pump activity. The reduction in ATP level and Na-K-ATPase activity may play a major role in damage to lung tissue following exposure to phosgene.
将大鼠置于罗切斯特型实验舱中，暴露于浓度为1.0 ppm的光气环境下4小时。此后在4天的时间段内，每隔一段时间获取大鼠的肺部组织，用于组织学和生化评估。通过组织学检查以及测量肺组织的湿重和干重来评估水肿情况。在平行研究中，使用克拉克氧电极测量肺线粒体呼吸活性。光气暴露后立即发现呼吸控制指数（状态3呼吸/状态4呼吸）显著降低，这与肺含水量的最高水平相一致。同时，ATP浓度降低，且在暴露后第三天仍持续存在。暴露1天后，钠钾ATP酶活性降低，因此在钠钾ATP酶或钠泵活性降低之前，ATP水平就已经下降。ATP水平和钠钾ATP酶活性的降低可能在光气暴露后肺组织损伤中起主要作用。
