Seibert A F, Taylor A E, Bass J B, Haynes J
Department of Medicine, University of South Alabama, Mobile 36617.
Am J Physiol. 1991 Jun;260(6 Pt 2):H1980-4. doi: 10.1152/ajpheart.1991.260.6.H1980.
Isolated perfused rat lungs were subjected to oxidant injury induced by tert-butyl hydroperoxide (t-buOOH), which caused a significant increase in capillary permeability as assessed by the change in the capillary filtration coefficient. t-buOOH caused an increase in the change in the capillary filtration coefficient (delta Kfc) of 0.27 +/- 0.05 ml.min.cmH2O-1.100 g lung tissue-1 (mean +/- SE) that was accompanied by an increase in thiobarbituric acid reactive products of lipid peroxidation in the lung perfusate. The addition of hemoglobin to the perfusate potentiated t-buOOH-induced lung injury as evidenced by a significantly greater (P = 0.007) delta Kfc of 0.43 +/- 0.05. t-buOOH also caused hemoglobin to release large quantities of free iron in vitro. The potentiation of t-buOOH-induced lung injury by hemoglobin was prevented by apotransferrin as evidenced by a significant reduction (P = 0.001) in delta Kfc to 0.13 +/- 0.02. No statistically significant (P greater than 0.05) changes in segmental resistances or pulmonary vascular pressures occurred in any of the lungs injured with t-buOOH when compared with time controls. These results demonstrate that t-buOOH causes an oxidant injury in isolated rat lungs that can be potentiated by free iron released from hemoglobin.
将离体灌注的大鼠肺脏暴露于叔丁基过氧化氢（t-buOOH）诱导的氧化损伤中，通过毛细血管滤过系数的变化评估发现，这会导致毛细血管通透性显著增加。t-buOOH使毛细血管滤过系数（ΔKfc）增加了0.27±0.05 ml·min·cmH₂O⁻¹·100 g肺组织⁻¹（平均值±标准误），同时肺灌注液中脂质过氧化的硫代巴比妥酸反应产物增加。向灌注液中添加血红蛋白会增强t-buOOH诱导的肺损伤，表现为ΔKfc显著增大（P = 0.007），达到0.43±0.05。t-buOOH在体外还会使血红蛋白释放大量游离铁。脱铁转铁蛋白可防止血红蛋白对t-buOOH诱导的肺损伤的增强作用，表现为ΔKfc显著降低（P = 0.001）至0.13±0.02。与时间对照组相比，用t-buOOH损伤的任何肺脏的节段阻力或肺血管压力均未发生统计学显著变化（P＞0.05）。这些结果表明，t-buOOH在离体大鼠肺脏中引起氧化损伤，血红蛋白释放的游离铁可增强这种损伤。
