DIFFERENTIAL PERMEABILITY OF ENDOTHELIAL AND EPITHELIAL BARRIERS TO ALBUMIN FLUX

DIFFERENTIAL PERMEABILITY OF ENDOTHELIAL AND EPITHELIAL BARRIERS TO ALBUMIN FLUX
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DOI:
10.1152/jappl.1979.47.6.1315
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发表时间:
1979-01-01
影响因子:
3.3
通讯作者:
STEWART, PA
STEWART, PA
中科院分区:
医学2区
文献类型:
--
作者:
GORIN, AB;STEWART, PA

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在20只患有慢性肺淋巴瘘的成年绵羊上,测定了白蛋白在血管间隙与肺间质和管腔衬里液之间的流量。通过间歇性纤维支气管镜灌洗对支气管肺泡衬里层进行取样。在动脉内注射100 μ Ci的125 I标记的白蛋白后30分钟至60小时的时间范围内进行总共62次肺泡灌洗。与灌洗液同时获得淋巴和血浆样品,测量所有样品的放射性和白蛋白含量,并表示为比活性(计数/分钟. g白蛋白)。通过该技术收集的肺泡灌洗液未被血浆或间质液蛋白显著污染。存在于肺泡灌洗液中的蛋白质以及存在于血浆中的蛋白质通过正常的扩散过程到达肺泡空间,而不是由于灌洗时发生的上皮膜损伤。肺上皮细胞对白蛋白的渗透性很小,但有限(4.3 × 104)。10-10 cm/s)。几乎所有(> 92%)的白蛋白穿过肺泡毛细血管膜的阻力都存在于上皮屏障中。呼吸道上皮通透性的增加,即使是轻微的,也会对肺中的水和溶质平衡产生显著影响。即使在肺微血管压、血浆内皮压和内皮通透性正常的情况下,上皮损伤也会促进肺水肿的形成。
The flux of albumin between the vascular space and the pulmonary interstitial and luminal lining fluids was measured in 20 adult sheep with chronic lung lymph fistulas. Bronchoalveolar lining layer was sampled by episodic fiberbronchoscopic lavage. A total of 62 alveolar lavages were performed at times ranging between 30 min and 60 h after intra-arterial injection of 100 .mu.Ci of 125I-labeled albumin. Samples of lymph and plasma were obtained simultaneously with lavage fluid, and the radioactivity and albumin content of all samples were measured and expressed as specific activity (counts/min .cntdot. g albumin). Alveolar lavage fluid collected by this technique is not significantly contaminated by plasma or interstitial fluid proteins. Proteins present in alveolar lavage fluid and also present in plasma reach the alveolar space by a normal diffusive process, and not as a result of epithelial membrane damage occurring at the time of lavage. Lung epithelial permeability to albumin is small, but finite (4.3 .times. 10-10 cm/s). Virtually all (> 92%) of resistance to albumin flux across the alveolocapillary membrane lies in the epithelial barrier. Increases in permeability of the respiratory epithelium, even minor, would have a marked effect on water and solute balance in the lung. Epithelial injury will potentiate pulmonary edema formation even in the presence of normal pulmonary microvascular pressure, plasma oncotic pressure and endothelial permeability.