Fein A, Grossman R F, Jones J G, Hoeffel J, McKay D
Chest. 1980 Nov;78(5):726-31. doi: 10.1378/chest.78.5.726.
A carbon monoxide (CO)-intoxicated patient developed increased permeability-type pulmonary edema demonstrated by a normal capillary wedge pressure and production of protein-rich edema fluid. To investigate the effect of CO on alveolar-epithelial permeability, a radio-active labelled isotope, 51Cr-EDTA (MW 377), was instilled into the airways of rabbits. Subsequent egress of the marker from the lungs into arterial blood was determined in serial arterial blood samples. The 51Cr-EDTA counts increased significantly within 15 minutes in the CO-exposed animals, compared with the control animals, while dynamic lung compliance fell, airways resistance rose, and arterial blood pressure decreased. Ultrastructural study of the lungs of CO-exposed animals revealed epithelial and endothelial cell swelling, in terstitial edema, and alveolar type II cells depleted of lamellar bodies. These findings support the possibility that carbon monoxide intoxication is associated with increased alveolar-epithelial permeability.
一名一氧化碳（CO）中毒患者出现了通透性增加型肺水肿，表现为毛细血管楔压正常且产生富含蛋白质的水肿液。为了研究CO对肺泡上皮通透性的影响，将放射性标记的同位素51Cr - EDTA（分子量377）注入兔气道。随后通过连续采集动脉血样本测定标记物从肺进入动脉血的流出情况。与对照动物相比，暴露于CO的动物在15分钟内51Cr - EDTA计数显著增加，同时动态肺顺应性下降、气道阻力升高且动脉血压降低。对暴露于CO的动物肺部进行超微结构研究发现上皮细胞和内皮细胞肿胀、间质水肿以及II型肺泡细胞板层小体减少。这些发现支持一氧化碳中毒与肺泡上皮通透性增加有关的可能性。
