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臭氧诱导的大鼠支气管高反应性并未伴有气管中中性粒细胞流入或血管通透性增加。

Ozone-induced bronchial hyperresponsiveness in the rat is not accompanied by neutrophil influx or increased vascular permeability in the trachea.

作者信息

Evans T W, Brokaw J J, Chung K F, Nadel J A, McDonald D M

机构信息

Cardiovascular Research Institute, University of California, San Francisco.

出版信息

Am Rev Respir Dis. 1988 Jul;138(1):140-4. doi: 10.1164/ajrccm/138.1.140.

DOI:10.1164/ajrccm/138.1.140
PMID:3202393
Abstract

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.

摘要

我们确定了大鼠中臭氧诱导的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臭氧2小时,随后立即进行研究;另一组同样暴露,但直到臭氧暴露后24小时才进行研究;第三组为吸入室内空气的对照大鼠。通过测量乙酰胆碱气雾剂引起的总肺阻力增加来评估这三组的支气管反应性。在平行研究中,通过对经组织化学处理以染色中性粒细胞中髓过氧化物酶的气管整装片内的细胞进行计数来量化中性粒细胞向气管黏膜的流入,并通过测量渗入气管的伊文思蓝染料量来量化气管血管通透性。在臭氧暴露后立即进行研究的大鼠中,使总肺阻力增加至基线值三倍所需的乙酰胆碱浓度仅为对照所需浓度的6%。在臭氧暴露后24小时进行研究的大鼠中,这种激发性乙酰胆碱浓度与对照相比无显著差异。在两个时间点,气管黏膜中的中性粒细胞数量或渗入气管的伊文思蓝染料量与相应的对照值均无显著差异。我们得出结论,暴露于臭氧的大鼠会出现支气管高反应性,而气管中未检测到中性粒细胞流入或血管通透性增加。

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