Matalon S, Cesar M A
Microvasc Res. 1985 Jan;29(1):70-80. doi: 10.1016/0026-2862(85)90007-x.
Prolonged exposure to 100% O2 at 1 atm is known to result in a progressive increase of the alveolar epithelial permeability to lipid-insoluble molecules. To investigate whether the damage to the capillary endothelium precedes or follows this event, conscious, unanesthetized rabbits were exposed to 100% O2 from 24 to 66 hr, and (a) the filtration coefficient (Kf) of the pulmonary capillary endothelium in isolated, perfused lungs and (b) the arterial and carbon dioxide gas tensions and right and left heart vascular pressures were measured in intact animals. The mean value of the filtration coefficient (+/- SEM) in air-breathing animals was 0.036 +/- 0.002 ml/(min x Torr x g dry lung). After 48 and 66 hr in 100% O2, it increased by 58 and 114% from its baseline value, respectively. At the later period the lung wet/dry weight of the isolated, but not the intact lungs, increased also from 5.42 +/- .2 to 7.3 +/- .3 (means +/- 1 SEM) due to the combination of a higher capillary conductance and the lack of lymph flow in this preparation. All other variables remained normal throughout the exposure. Thus, in contrast to previous morphological findings, these results indicate that the oxygen damage to the capillary endothelium is progressive and occurs concurrently with the increase of the alveolar permeability to solute but before the appearance of pulmonary edema and the compromise of gas exchange.
已知在1个大气压下长时间暴露于100%氧气会导致肺泡上皮对脂溶性分子的通透性逐渐增加。为了研究毛细血管内皮损伤是先于还是后于这一事件发生,将清醒、未麻醉的兔子暴露于100%氧气中24至66小时,并在(a)分离的灌注肺中测量肺毛细血管内皮的滤过系数(Kf),以及在(b)完整动物中测量动脉和二氧化碳气体张力以及左右心血管压力。呼吸空气的动物的滤过系数(±标准误)的平均值为0.036±0.002 ml/(min·Torr·g干肺)。在100%氧气中暴露48小时和66小时后,其分别比基线值增加了58%和114%。在后期,由于该制备中毛细血管传导性较高且缺乏淋巴液流动,分离的肺(而非完整的肺)的湿/干重也从5.42±0.2增加到7.3±0.3(平均值±1标准误)。在整个暴露过程中,所有其他变量均保持正常。因此,与先前的形态学研究结果相反,这些结果表明,氧气对毛细血管内皮的损伤是渐进性的,与肺泡对溶质通透性的增加同时发生,但在肺水肿出现和气体交换受损之前。