Perkins Michael W, Wong Benjamin, Tressler Justin, Rodriguez Ashley, Sherman Katherine, Andres Jaclynn, Devorak Jennifer, L Wilkins William, Sciuto Alfred M
a US Army Medical Research Institute of Chemical Defense , Aberdeen Proving Ground , MD , USA.
Inhal Toxicol. 2017 Jan;29(1):32-41. doi: 10.1080/08958378.2016.1277571.
Acute respiratory dynamics and histopathology of the lungs and trachea following inhaled exposure to ammonia were investigated. Respiratory dynamic parameters were collected from male Sprague-Dawley rats (300-350 g) during (20 min) and 24 h (10 min) after inhalation exposure for 20 min to 9000, 20,000, and 23,000 ppm of ammonia in a head-only exposure system. Body weight loss, analysis of blood cells, and lungs and trachea histopathology were assessed 1, 3, and 24 h following inhalation exposure to 20,000 ppm of ammonia. Prominent decreases in minute volume (MV) and tidal volume (TV) were observed during and 24 h post-exposure in all ammonia-exposed animals. Inspiratory time (IT) and expiratory time (ET) followed similar patterns and decreased significantly during the exposure and then increased at 24 h post-exposure in all ammonia-exposed animals in comparison to air-exposed controls. Peak inspiratory (PIF) and expiratory flow (PEF) significantly decreased during the exposure to all ammonia doses, while at 24 h post-exposure they remained significantly decreased following exposure to 20,000 and 23,000 ppm. Exposure to 20,000 ppm of ammonia resulted in body weight loss at 1 and 3 h post-exposure; weight loss was significant at 24 h compared to controls. Exposure to 20,000 ppm of ammonia for 20 min resulted in increases in the total blood cell counts of white blood cells, neutrophils, and platelets at 1, 3, and 24 h post-exposure. Histopathologic evaluation of the lungs and trachea tissue of animals exposed to 20,000 ppm of ammonia at 1, 3, and 24 h post-exposure revealed various morphological changes, including alveolar, bronchial, and tracheal edema, epithelial necrosis, and exudate consisting of fibrin, hemorrhage, and inflammatory cells. The various alterations in respiratory dynamics and damage to the respiratory system observed in this study further emphasize ammonia-induced respiratory toxicity and the relevance of efficacious medical countermeasure strategies.
研究了吸入氨气后肺和气管的急性呼吸动力学及组织病理学变化。在头部暴露系统中，将雄性Sprague-Dawley大鼠（300 - 350克）暴露于9000、20000和23000 ppm的氨气中20分钟，然后在暴露期间（20分钟）和暴露后24小时（10分钟）收集呼吸动力学参数。在暴露于20000 ppm氨气后1、3和24小时，评估体重减轻、血细胞分析以及肺和气管组织病理学变化。在所有氨气暴露动物中，暴露期间和暴露后24小时观察到分钟通气量（MV）和潮气量（TV）显著降低。吸气时间（IT）和呼气时间（ET）呈现相似模式，与空气暴露对照组相比，所有氨气暴露动物在暴露期间显著缩短，暴露后24小时延长。在暴露于所有氨气剂量期间，吸气峰流速（PIF）和呼气峰流速（PEF）显著降低，而在暴露后24小时，暴露于20000和23000 ppm氨气后它们仍显著降低。暴露于20000 ppm氨气导致暴露后1和3小时体重减轻；与对照组相比，24小时时体重减轻显著。暴露于20000 ppm氨气20分钟导致暴露后1、3和24小时白细胞、中性粒细胞和血小板的总血细胞计数增加。暴露于20000 ppm氨气后1、3和24小时对动物肺和气管组织的组织病理学评估显示出各种形态学变化，包括肺泡、支气管和气管水肿、上皮坏死以及由纤维蛋白、出血和炎性细胞组成的渗出物。本研究中观察到的呼吸动力学的各种改变以及呼吸系统的损伤进一步强调了氨气诱导的呼吸毒性以及有效医学对策策略的相关性。
