Vlcková A, Takác L
Sci Total Environ. 1975 Sep;4(3):311-5. doi: 10.1016/0048-9697(75)90008-x.
Rats of two age groups, of 119 and 163 g mean body weight, were exposed for three and thirty days, respectively, to automobile gases diluted with air. In addition, rabbits, of 1.88 kg mean body weight, were exposed for twenty-four days. The conditions of exposure were kept nearly constant as related to the concentration of CO in the chamber. The following determinations were performed: (1) Body weight measurements as evidence of growth of the animals; (2) The number of alveolar macrophages (AM) in the lung washings; (3) Damage to the integrity of the cytoplasmic membrane of AM; (4) Glucose-6-phosphate dehydrogenase activity (G6PD) in AM; (5) The acid-base balance in the capillary blood of the rabbits. The results of the 30-day exposure show that automobile exhaust gases significantly inhibit the growth of both age groups; with significant body weight losses in the older animals from the 16th day of exposure. The number of AM was elevated in both groups. The activity of G6PD increased in the AM of the younger animals and decreased in the AM of the older as compared with the controls. The number of dead AM was higher in the older than in the younger rats. After the three-day exposure, no significant difference was found in the number of AM washed from the lungs of both exposed groups, compared with the controls. However, G6PD activity and the number of viable AM in the older animals were decreased and the percent of dead phagocytes was significant. The opposite effect was seen in the younger group. Alterations of lung tissue structure in the exposed animals were apparent to the naked eye. Acid-base response showed metabolic and respiratory disturbances as evidenced by the decrease in carbon dioxide tension (PCo2), the rise of hemoglobin by the reduction of pH level and by the base excess (BE). The inhibition of the growth of the rabbits was noted. The intra- and extrapulmonary effect of automobile exhaust gases after inhalation was observed as a complex of disturbances of the fundamental metabolic processes in the organism. The gases affected the cells of lung defence-alveolar macrophages and their biosynthetic activity.
将两组平均体重分别为119克和163克的大鼠,分别暴露于用空气稀释的汽车尾气中3天和30天。此外,将平均体重为1.88千克的兔子暴露24天。暴露条件与室内一氧化碳浓度相关,几乎保持恒定。进行了以下测定:(1) 测量体重以证明动物的生长情况;(2) 测定肺灌洗液中肺泡巨噬细胞(AM)的数量;(3) 检测AM细胞质膜完整性的损伤情况;(4) 测定AM中的葡萄糖-6-磷酸脱氢酶活性(G6PD);(5) 检测兔子毛细血管血中的酸碱平衡。30天暴露的结果表明,汽车尾气显著抑制了两个年龄组大鼠的生长;老年动物从暴露第16天起体重显著减轻。两组的AM数量均增加。与对照组相比,幼年动物AM中的G6PD活性增加,老年动物AM中的G6PD活性降低。老年大鼠中死亡AM的数量高于幼年大鼠。暴露3天后,与对照组相比,两个暴露组从肺中洗出的AM数量没有显著差异。然而,老年动物中G6PD活性和存活AM数量减少,死亡吞噬细胞百分比显著增加。幼年组则出现相反的效果。肉眼可见暴露动物的肺组织结构发生改变。酸碱反应显示出代谢和呼吸紊乱,表现为二氧化碳分压(PCo2)降低、pH值降低导致血红蛋白升高以及碱剩余(BE)升高。观察到兔子的生长受到抑制。吸入汽车尾气后,其在肺内和肺外的作用表现为机体基本代谢过程的一系列紊乱。这些气体影响了肺防御细胞——肺泡巨噬细胞及其生物合成活性。