OZONE-INDUCED BRONCHIAL HYPERRESPONSIVENESS IN THE RAT IS NOT ACCOMPANIED BY NEUTROPHIL INFLUX OR INCREASED VASCULAR-PERMEABILITY IN THE TRACHEA
OZONE-INDUCED BRONCHIAL HYPERRESPONSIVENESS IN THE RAT IS NOT ACCOMPANIED BY NEUTROPHIL INFLUX OR INCREASED VASCULAR-PERMEABILITY IN THE TRACHEA
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DOI：
10.1164/ajrccm/138.1.140
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发表时间：
1988-07-01
期刊：
影响因子：
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通讯作者：
MCDONALD, DM
中科院分区：
文献类型：
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作者：
EVANS, TW;BROKAW, JJ;MCDONALD, DM
我们确定臭氧诱导的大鼠支气管高反应性是否伴有中性粒细胞流入或气管血管通透性增加。研究了三组雌性Long-Evans大鼠。一组暴露于4 ppm的臭氧2小时，并在此后立即进行研究，另一组同样暴露，但直到24小时后才进行研究，第三组由对照大鼠呼吸室内空气。测量乙酰胆碱气雾剂引起的总肺阻力增加，以评估这3组的支气管反应性。在平行研究中，通过计数经组织化学处理以染色中性粒细胞中的髓过氧化物酶的整个气管内的细胞来定量中性粒细胞流入气管粘膜，并通过测量外渗到气管中的伊文思蓝染料的量来定量气管血管通透性。在臭氧暴露后立即研究的大鼠中，将总肺阻力增加到基线值的三倍所需的乙酰胆碱浓度仅为对照组所需的6%。在臭氧暴露后24小时研究的大鼠中，这种挑衅性的乙酰胆碱浓度与对照组没有显着差异。在任一时间，气管粘膜中的中性粒细胞数量和外渗到气管中的伊文思蓝染料量与相应的对照值均无显著差异。我们的结论是，大鼠暴露于臭氧发展支气管高反应性没有可检测到的中性粒细胞流入或增加气管血管通透性。
We determined whether ozone-induced bronchial hyperresponsiveness in the rat is accompanied by neutrophil influx or increased vascular permeability in the trachea. Three groups of female Long-Evans rats were studied. One group was exposed to 4 ppm ozone for 2 h and studied immediately thereafter, another group was similarly exposed but was not studied until 24 h after the ozone exposure, and a third group consisted of control rats that breathed room air. Increases in total pulmonary resistance caused by acetylcholine aerosol were measured to assess bronchial responsiveness in these 3 groups. In parallel studies, neutrophil influx into the tracheal mucosa was quantified by counting cells within whole mounts of tracheas that were treated histochemically to stain the myeloperoxidase in neutrophils, and tracheal vascular permeability was quantified by measuring the amount of Evans blue dye extravasated into the trachea. In the rats studied immediately after the ozone exposure, the concentration of acetylcholine required to increase total pulmonary resistance to three-fold the baseline value was only 6% of that required in the controls. In the rats studied 24 h after the ozone exposure, this provocative acetylcholine concentration was not significantly different from that of the controls. Neither the number of neutrophils in the tracheal mucosa nor the amount of Evans blue dye extravasated into the trachea was significantly different from the corresponding control values at either time. We conclude that rats exposed to ozone develop bronchial hyperresponsiveness without detectable neutrophil influx or increased vascular permeability in the trachea.