Folkesson H G, Kheradmand F, Matthay M A
Cardiovascular Research Institute, University of California San Francisco, 94143-0130.
Am J Respir Crit Care Med. 1994 Dec;150(6 Pt 1):1555-63. doi: 10.1164/ajrccm.150.6.7952614.
The effect of hyperosmolar fluid aspiration (seawater) on lung fluid balance has not been well studied. Therefore, the effect of this clinically relevant form of acute lung injury on the alveolar epithelial and lung endothelial barriers was examined in ventilated, anesthetized rabbits. Seawater (4 ml/kg body weight, 881 +/- 29 mOsm/kg) with 3 microCi of 125I-albumin was instilled into the lower trachea of ventilated, anesthetized rabbits. Osmotic equilibration with plasma was completed within the first 5 min after seawater instillation. In parallel with the osmotic equilibration of the seawater in the air spaces, there was a 3-fold dilution of the alveolar protein tracer 125I-albumin, indicating an initial large (300%) increase in alveolar fluid volume. There was a marked decline in arterial oxygenation at the same time that the alveolar fluid volume markedly increased. The initial dilution of the alveolar protein tracer was followed by a progressive increase in the alveolar protein tracer concentration that continued until 6 h after seawater instillation. As the alveolar protein tracer concentrated, arterial oxygenation improved, indicting net alveolar liquid clearance. There was only a mild increase in the epithelial and endothelial permeability to protein within the first 2 h after seawater instillation. Thus, a large osmotically induced increase in alveolar fluid volume with severe pulmonary edema did not cause sustained injury to the endothelial or epithelial barriers of the lung. In fact, normal alveolar liquid clearance occurred, indicating the resistance of the epithelial barrier to hyperosmolar injury as well as its capacity to rapidly reabsorb excess alveolar fluid.
高渗液体吸入（海水）对肺液体平衡的影响尚未得到充分研究。因此，在通气的麻醉兔中研究了这种临床相关形式的急性肺损伤对肺泡上皮和肺内皮屏障的影响。将含有3微居里125I-白蛋白的海水（4毫升/千克体重，881±29毫渗量/千克）滴入通气的麻醉兔的下气管。海水滴入后最初5分钟内完成与血浆的渗透平衡。与气腔内海水的渗透平衡同时，肺泡蛋白示踪剂125I-白蛋白稀释了3倍，表明肺泡液体量最初大幅增加（300%）。在肺泡液体量显著增加的同时，动脉氧合明显下降。肺泡蛋白示踪剂最初稀释后，其浓度逐渐升高，一直持续到海水滴入后6小时。随着肺泡蛋白示踪剂浓度升高，动脉氧合改善，表明肺泡液体净清除。海水滴入后最初2小时内，上皮和内皮对蛋白的通透性仅轻度增加。因此，渗透压诱导的肺泡液体量大幅增加伴严重肺水肿并未对肺内皮或上皮屏障造成持续性损伤。事实上，出现了正常的肺泡液体清除，表明上皮屏障对高渗损伤具有抵抗力，以及其快速重吸收过量肺泡液体的能力。
