ULTRASTRUCTURE OF ACUTE AMMONIA TOXICITY IN THE HUMAN-LUNG

ULTRASTRUCTURE OF ACUTE AMMONIA TOXICITY IN THE HUMAN-LUNG
复制标题

DOI:
10.1097/00000433-198509000-00006
复制
发表时间:
1985-01-01
影响因子:
1
通讯作者:
JACHIMCZYK, JA
JACHIMCZYK, JA
中科院分区:
医学4区
文献类型:
--
作者:
BURNS, TR;MACE, ML;JACHIMCZYK, JA

文献摘要

被引文献

相似文献

一辆载有无水氨(NH 3)的油罐车从高速公路上坠落,释放出大量NH 3气体,造成数人死亡。司机在撞击时死亡。据我们所知,肺氨毒性在人类还没有研究以前的电子显微镜(EM)。因此,在2例病例中,将石蜡包埋的肺组织块脱蜡并重新包埋在塑料中,用于1-μ切片和EM检查。第三个病例,卡车司机的肺组织,作为对照进行了类似的处理。急性NH3死亡的光镜肺部发现包括气管支气管上皮剥脱、固有层水肿和明显的肺泡水肿、充血和出血。相比之下,在卡车司机的肺,支气管上皮细胞是完整的,没有明显的气味的氨3。他肺部的大量肺水肿是由于创伤而不是NH3吸入造成的。卡车司机肺部的EM检查显示,毛细血管内皮细胞或I型或II型肺泡上皮细胞均无明显毒性改变,肺泡和毛细血管基底膜完整。与此相反,EM研究的两个人的肺急性死亡的NH3吸入显示显着肿胀和吸入性水肿的I型肺泡上皮细胞,但肺泡基底膜和毛细血管内皮细胞出现如常。电镜结果表明,Ⅰ型上皮细胞是NH3吸入致肺泡壁损伤的靶细胞。
A tanker truck carrying anhydrous ammonia (NH 3) fell off a freeway, releasing a dense cloud of NH 3 gas, killing several people. The driver was dead upon impact. To our knowledge, pulmonary NH 3 toxicity in humans has not been studied previously by electron microscopy (EM). Therefore, in two cases, the paraffin-embedded tissue blocks of lung were deparaffinized and reembedded in plastic for 1-μ sections and EM examination. The lung tissue of a third case, the truck driver, was similarly processed as a control. Light-microscopic pulmonary findings in the acute NH 3 deaths included denudation of the tracheobronchial epithelium, edema of the lamina propria, and marked alveolar edema, congestion, and hemorrhage. In contrast, in the truck driver's lungs, the bronchial epithelium was intact, and there was no gross odor of NH 3. Massive pulmonary hemorrhages in his lungs were attributed to trauma rather than NH 3 inhalation. EM examination of the lungs of the truck driver showed no discernible toxic alterations in either the capillary endothelial cells or the Type I or II alveolar epithelial cells, and alveolar and capillary basement membranes were intact. In contrast, EM study of the lungs from two individuals dying acutely of NH 3 inhalation showed marked swelling and imbitional edema of Type I alveolar epithelial cells; however, alveolar basement membranes and capillary endothelial cells appeared as usual. These electron-microscopic findings demonstrate the Type I epithelial cell to be the target cell of acute alveolar wall injury in NH 3 inhalation.