Fox R B, Hoidal J R, Brown D M, Repine J E
Am Rev Respir Dis. 1981 May;123(5):521-3. doi: 10.1164/arrd.1981.123.5.521.
Although the pathogenesis of pulmonary oxygen toxicity is not fully understood, the fact that increased numbers of polymorphonuclear leukocytes (PMN) are found in the lung and that these increases coincide with the massive endothelial damage raises the possibility that PMN may contribute to lung injury caused by hyperoxia. In order to begin to elucidate a mechanism for this influx of PMN, we measured the chemoattractant activity for PMN of lung lavages of rats exposed to greater than 95% oxygen for various durations. We found that the chemoattractant activity of the lavages of the lungs of rats exposed to hyperoxia for 66 h was markedly increased (9.66 +/- 1.0 times greater) compared with activities in lavages of normoxic control rats. Furthermore, these increases in chemoattractant activity in lung lavages correlated well with increases in the number of PMN (7 times greater than that in normoxic control animals) in the alveolar lavages that occurred after the rats had been exposed to hyperoxia for 66 h. These increases were followed in a few hours by the death of most of the rats (71%). These findings suggested that a close temporal relationship exists between the generation of high concentrations of chemoattractants in lung lavages, PMN influx into lung lavages, and death of rats exposed to hyperoxia. The results supported the possibility that PMN may be involved in the pathogenesis of pulmonary oxygen toxicity.
虽然肺氧中毒的发病机制尚未完全明了，但在肺中发现多形核白细胞（PMN）数量增加，且这些增加与大量内皮损伤同时出现，这增加了PMN可能导致高氧引起的肺损伤的可能性。为了开始阐明PMN这种流入的机制，我们测量了暴露于大于95%氧气不同时长的大鼠肺灌洗物对PMN的趋化活性。我们发现，与常氧对照大鼠灌洗物中的活性相比，暴露于高氧66小时的大鼠肺灌洗物的趋化活性显著增加（高9.66±1.0倍）。此外，肺灌洗物中趋化活性的这些增加与大鼠暴露于高氧66小时后肺泡灌洗物中PMN数量的增加（比常氧对照动物高7倍）密切相关。在几小时后，大多数大鼠（71%）死亡。这些发现表明，肺灌洗物中高浓度趋化因子的产生、PMN流入肺灌洗物以及暴露于高氧的大鼠死亡之间存在密切的时间关系。结果支持了PMN可能参与肺氧中毒发病机制的可能性。
