Dormans J A, van Bree L, Boere A J, Marra M, Rombout P J
Laboratory for Pathology, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands.
J Toxicol Environ Health. 1989;26(1):1-18. doi: 10.1080/15287398909531230.
The effects of short-term exposure to ozone on control and elastase-induced emphysematous rats were examined to investigate whether emphysema would change the pulmonary susceptibility to oxidant air pollution. Emphysema was induced in rats after a single intratracheal instillation of 0.2 IU elastase/g body weight. Histologically, panacinar emphysema was apparent at 2, 4, 8, and 16 wk, that is, the total duration of the experiment. The diagnosis was confirmed by morphometry: the mean linear intercepts (MLI) of elastase-treated rats were significantly increased at all observation times, whereas the internal surface areas (ISA) of the elastase-treated rats were significantly decreased. In addition, pulmonary function tests provided supportive evidence for the diagnosis of emphysema. Respiratory system compliance and functional residual capacity showed a significant increase in elastase-treated rats. No differences in inspiratory capacity or in forced vital capacity between control rats and elastase-treated rats were observed. The above data are indicative for a rat model for elastase-induced emphysema. Short-term exposure to ozone of elastase-treated rats revealed panacinar emphysema, including an inflammatory response in the centroacinar region. No differences in MLI as well as in ISA between ozone-exposed rats (with or without emphysema) and their respective controls were observed. Short-term exposure to ozone induced an identical, significant increase in protein content, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, and glutathione peroxidase activities in lungs of normal and emphysematous rats. Moreover, these results strongly suggest that emphysematous rats are not more susceptible to ozone than nonemphysematous rats.
研究短期暴露于臭氧对正常大鼠和弹性蛋白酶诱导的肺气肿大鼠的影响，以探讨肺气肿是否会改变肺部对氧化性空气污染的易感性。在大鼠气管内单次注入0.2 IU弹性蛋白酶/克体重后诱导肺气肿。组织学上，在实验的整个持续时间即2、4、8和16周时，全腺泡型肺气肿明显。通过形态计量学证实了诊断：弹性蛋白酶处理的大鼠在所有观察时间的平均线性截距（MLI）均显著增加，而弹性蛋白酶处理的大鼠的内表面积（ISA）显著降低。此外，肺功能测试为肺气肿的诊断提供了支持性证据。弹性蛋白酶处理的大鼠的呼吸系统顺应性和功能残气量显著增加。未观察到正常大鼠和弹性蛋白酶处理的大鼠在吸气量或用力肺活量方面存在差异。上述数据表明建立了弹性蛋白酶诱导的肺气肿大鼠模型。弹性蛋白酶处理的大鼠短期暴露于臭氧后出现全腺泡型肺气肿，包括中心腺泡区域的炎症反应。暴露于臭氧的大鼠（有或没有肺气肿）与其各自的对照组在MLI以及ISA方面没有差异。正常大鼠和肺气肿大鼠肺部的蛋白质含量、乳酸脱氢酶、葡萄糖-6-磷酸脱氢酶和谷胱甘肽过氧化物酶活性在短期暴露于臭氧后均出现相同的显著增加。此外，这些结果强烈表明，肺气肿大鼠对臭氧的易感性并不高于非肺气肿大鼠。
