Acute bronchiolar injury following nitrogen dioxide exposure: a freeze fracture study.
Acute bronchiolar injury following nitrogen dioxide exposure: a freeze fracture study.
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二氧化氮暴露后的急性细支气管损伤：冷冻骨折研究。
DOI：
10.1016/0013-9351(82)90041-x
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发表时间：
1982
影响因子：
8.3
通讯作者：
Kleinerman,J
中科院分区：
文献类型：
--
作者：
Case,BW;Gordon,RE;Kleinerman,J
三组叙利亚金仓鼠暴露于 NO2 6、24 或 48 小时，以确定对远端气道和肺泡上皮细胞间连接形态的急性影响。第四组暴露 48 小时，在处死前恢复 2 天。细支气管上皮的光学和透射电子显微镜显示纤毛损失和表面膜损伤、纤毛细胞损失以及24和48小时时上皮变平。 48小时后观察到中度至显着的上皮增生和非纤毛细胞肥大。在允许 48 小时恢复期的动物细支气管中注意到正常组织结构的一些恢复。细支气管上皮的冷冻断裂铂-碳复制品显示，暴露 6、24 和 48 小时后，紧密连接网络逐渐受到严重破坏。经过 2 天的“恢复”后，暴露 48 小时的动物的细支气管紧密连接仍然支离破碎。存在的连接材料的广泛分布表明存在再生过程。支气管上皮的冷冻断裂复制品在暴露 6 小时后显示出类似的紧密连接碎片。然而，经过较长时间的间隔后，外观会恢复到更正常的状态。 NO2 暴露时间对肺泡上皮紧密连接的完整性没有系统性影响。研究结果表明，紧密连接的破坏可能是短暂暴露于二氧化氮后细支气管上皮通透性增加的一个重要的具体决定因素。
Three groups of Syrian golden hamsters were exposed to NO2for 6, 24, or 48 hr to determine acute effects on intercellular junctional morphology in distal airways and alveolar epithelium. A fourth group, exposed for 48 hr, was allowed to recover for 2 days prior to sacrifice. Light and transmission electron microscopy of bronchiolar epithelium show ciliary loss and surface membrane damage, loss of ciliated cells, and epithelial flattening at 24 and 48 hr. Moderate to marked epithelial hyperplasia and nonciliated cell hypertrophy are noted after 48 hr. Some restoration of normal histoarchitecture is noted in bronchioles of animals allowed a 48-hr recovery period. Freeze fracture platinum-carbon replicas of bronchiolar epithelium show the gradual evolution of a severe disruption of tight junctional networks after 6, 24, and 48 hr of exposure. Following 2 days of “recovery,” bronchiolar tight junctions from animals exposed for 48 hr remain fragmented. The wide distribution of the junctional material present suggests a regenerative process. Freeze fracture replicas of bronchial epithelium show similar fragmentation of tight junctions following 6-hr exposures. After longer intervals, however, there is a return to more normal appearances. Duration of NO2exposure has no systematic effect on the integrity of tight junctions in alveolar epithelium. The findings suggest that disruption of tight junctions may be an important specific determinant of increased bronchiolar epithelial permeability following brief exposures to nitrogen dioxide.