Pathologic changes in rat lungs following acute sulfur mustard inhalation
Pathologic changes in rat lungs following acute sulfur mustard inhalation
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DOI：
10.3109/08958379609005436
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发表时间：
1996-04-01
影响因子：
2.1
通讯作者：
Byers, SL
中科院分区：
文献类型：
--
作者：
Anderson, DR;Yourick, JJ;Byers, SL
虽然暴露于硫芥菜（HD）造成的大多数死亡是由于肺功能障碍，但没有详细的发病机制或HD引起的呼吸道病变。因此，我们研究了吸入HD后大鼠气管和肺部的早期变化。麻醉大鼠经气管插管暴露于汽化HD （0.35 mg / 100 μ l无水乙醇）或单独乙醇中50分钟。分别于暴露后0、1、4、6、12、18和24 h对动物实施安乐死，并对其呼吸道进行组织学和超微结构检查。暴露于HD的大鼠，肺胸膜表面多灶性点状出血在PE 6 h时非常明显。术后12-18 h副叶出现肺不张和水肿。组织学上，呼吸道病变主要局限于气管、支气管和较大的细支气管。在hd暴露的大鼠中，细支气管相关淋巴组织（BALT）出现进行性耗竭，淋巴样细胞早在12小时就出现坏死。6-12 h气管和支气管上皮坏死和脱落，支气管内纤维性假膜形成。粘膜/粘膜下界面出现气道上皮坏死和分离。假膜几乎只在BALT上的深度上皮化区域形成。软骨病变，以单个软骨细胞坏死为特征，在12小时PE时很明显。肺水肿，肺泡出血偶有发生。小细支气管和肺泡相对未受影响，任何时间仅观察到少量炎症细胞。
Although the majority of deaths resulting from exposure to sulfur mustard (HD) have been due to pulmonary dysfunction, there are no detailed accounts of the pathogenesis or HD-induced lesions in the respiratory tract. Accordingly, we investigated the early changes within the trachea and lungs of rats following inhalation exposure to HD. Anesthetized rats were exposed by intratracheal intubation to vaporized HD (0.35 mg in 100 mu l absolute ethanol) or ethanol alone for 50 min. Animals were euthanatized at 0, 1, 4, 6, 12, 18, and 24 h postexposure (PE), and their respiratory tracts were prepared for histological and ultrastructural examination. In rats exposed to HD, multifocal, petechial hemorrhages were grossly evident on the pleural surface of the lung at 6 h PE. Atelectasis and edema of the accessory lobe occurred at 12-18 h PE. Histologically, lesions in the respiratory tract were confined primarily to the trachea, bronchi and larger bronchioles. In HD-exposed rats, there was a progressive depletion of the bronchiolar-associated lymphoid tissue (BALT), with necrosis of the lymphoid cells as early as 12 h PE. Necrosis and sloughing of the tracheal and bronchial epithelia at 6-12 h PE was followed by the formation of fibrinous pseudomembranes within the bronchi. Necrosis and separation of airway epithelia occurred at the mucosal/submucosal interface. Pseudomembranes formed almost exclusively in deepithelialized areas overlying the BALT. Cartilaginous lesions, characterized by necrosis of individual chondrocytes, were evident at 12 h PE. Pulmonary edema and occasional alveolar hemorrhage occurred from 18 to 24 h PE. Small bronchioles and alveoli were relatively unaffected and only a few inflammatory cells were observed at any time.