Sequence of pathologic changes in the airway mucosa of guinea pigs during ozone-induced bronchial hyperreactivity.
Sequence of pathologic changes in the airway mucosa of guinea pigs during ozone-induced bronchial hyperreactivity.
复制标题
臭氧引起的支气管高反应期间豚鼠气道粘膜病理变化的序列。
DOI：
10.1164/arrd.1985.131.3.314
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Roum,JH
中科院分区：
文献类型：
--
作者：
Murlas,CG;Roum,JH
我们评估了4只豚鼠在臭氧暴露后2小时、6小时、14小时、1天、2天或4天(3.0ppm，持续2小时)和1个对照组的呼吸道粘膜疾病和M支气管反应性的性质和进展。在31只完整的、未麻醉的、自主呼吸的动物中，通过测量比气道阻力随静脉注射乙酰胆碱剂量的增加来确定毒碱的反应性。检测结束后，处死各组动物，取气管组织进行光镜检查。我们发现，暴露在臭氧中的动物中，96%的动物对乙酰胆碱产生了高反应性。它在2小时时的程度是实质性的。直到第四天才观察到完全缓解。与2小时出现的急性支气管高反应性有关，呼吸道粘膜杯状细胞显著减少，粘膜肥大细胞增多。尽管高反应性缓解，但中性粒细胞渗入发生较晚且持续时间较长。我们的结果表明，臭氧诱导的急性支气管高反应性与呼吸道粘膜损伤和肥大细胞浸润的体征有关。在呼吸道损伤的早期阶段，中性粒细胞渗入发生并持续存在，这表明这是损伤的结果，而不是臭氧暴露后呼吸道反应性增加的原因。
We assessed the nature and progression of airway mucosal disease and muscarinic bronchial reactivity in guinea pigs studied in groups of 4 at 2 h, 6 h, 14 h, 1 day, 2 days, or 4 days after ozone exposure (3.0 ppm for 2 h), and in 1 control group. Muscarinic reactivity was determined by measuring specific airway resistance as a function of increasing doses of intravenous acetylcholine in 31 intact, unanesthetized, spontaneously breathing animals. After testing, each group was killed to obtain tracheal tissue for light microscopic examination. We found that airway hyperreactivity to acetylcholine occurred in 96% of the animals exposed to ozone. Its degree at 2 h was substantial. Complete remission was not observed until the fourth day. In association with the acute bronchial hyperreactivity found at 2 h, a marked decrease in airway mucosal goblet cells and an increase in mucosal mast cells occurred. Neutrophilic infiltration occurred later and lasted longer, despite remission of the hyperreactivity. Our results indicate that acute, ozone-induced bronchial hyperreactivity is related to signs of airway mucosal injury and mast cell infiltration. After this early phase of airway damage, neutrophilic infiltration occurs and persists, suggesting that it is a consequence of the damage rather than a cause of the increased airway reactivity after ozone exposure.