Goad M E, Tryka A F, Witschi H P
Toxicol Appl Pharmacol. 1987 Aug;90(1):10-22. doi: 10.1016/0041-008x(87)90301-2.
The acute manifestations of experimental bleomycin- and hyperoxia-induced lung damage were examined. Hamsters were treated with 5 U/kg bleomycin intratracheally followed by exposure to 80% oxygen (O2). As little as 12 hr of O2 exposure potentiated the bleomycin injury; however, the onset of mortality was 72 hr after treatment. The onset of pulmonary edema, measured by radiolabeled tracers, also occurred 72 hr after treatment. Cell kinetics studies showed that 24 hr exposure to 80% O2 did not alter early alveolar cell proliferation. Treatment with bleomycin alone did result in an early increase in alveolar macrophage and type II pneumocyte labeling. Animals treated with both bleomycin and hyperoxia had an increase in macrophage labeling, but not in type II pneumocyte labeling. We conclude that increased macrophage numbers associated with suppressed type II pneumocyte proliferation may play key roles in the potentiation and development of lung damage caused by bleomycin and hyperoxia treatment.
对实验性博来霉素和高氧诱导的肺损伤的急性表现进行了研究。仓鼠经气管内给予5 U/kg博来霉素，随后暴露于80%氧气（O2）中。仅12小时的氧气暴露就增强了博来霉素的损伤作用；然而，死亡发生在治疗后72小时。通过放射性标记示踪剂测量的肺水肿也在治疗后72小时出现。细胞动力学研究表明，暴露于80%氧气24小时并未改变早期肺泡细胞增殖。单独使用博来霉素治疗确实导致肺泡巨噬细胞和II型肺泡上皮细胞标记早期增加。同时接受博来霉素和高氧治疗的动物巨噬细胞标记增加，但II型肺泡上皮细胞标记未增加。我们得出结论，与II型肺泡上皮细胞增殖受抑制相关的巨噬细胞数量增加可能在博来霉素和高氧治疗引起的肺损伤的增强和发展中起关键作用。
