Tyler D C, Pavlin D J, Boatman E S, Nessly M, Cheney F W
Pediatr Pulmonol. 1986 Mar-Apr;2(2):75-81. doi: 10.1002/ppul.1950020204.
We investigated the effects of varying inspired oxygen concentrations on the resolution of oleic acid-induced lung injury in rabbits. Rabbits were injected intravenously with oleic acid and maintained in room air, or exposed to 60, 70, or 80% oxygen for periods of 7 or 10 days. Oleic acid caused hemorrhagic pulmonary edema with hypoxemia. Hypoxemia was more profound in the oxygen-treated animals, a difference that was significant after 7 days' exposure to 60 and 70% oxygen, and after 4 days to 80% oxygen. Mortality was increased in the animals maintained in 80% oxygen. The data suggest that environmental oxygen concentrations greater than 60% interfere with the return to normal lung function following oleic acid injury in rabbits. The hypoxemia may be due to either mismatching of ventilation and perfusion or to a diffusion block resulting from the increased septal width. There was no evidence of massive pulmonary edema as a cause of the hypoxemia. It was not possible to distinguish between injury primarily caused by oxygen and its interference with the healing process.
我们研究了不同吸入氧浓度对油酸诱导的兔肺损伤恢复的影响。给兔静脉注射油酸,使其置于室内空气中,或暴露于60%、70%或80%的氧气环境中7天或10天。油酸导致出血性肺水肿并伴有低氧血症。在吸氧治疗的动物中,低氧血症更为严重,在暴露于60%和70%氧气7天后,以及暴露于80%氧气4天后,这种差异具有显著性。维持在80%氧气环境中的动物死亡率增加。数据表明,环境氧浓度大于60%会干扰兔油酸损伤后肺功能恢复正常。低氧血症可能是由于通气与灌注不匹配,或由于间隔宽度增加导致的弥散障碍。没有证据表明大量肺水肿是低氧血症的原因。无法区分主要由氧气引起的损伤及其对愈合过程的干扰。