Animal model of status asthmatics.

为了探讨炎症细胞在晚期哮喘反应中的作用，我们对美托皮龙(皮质醇合成抑制剂)处理的犬进行了猪蛔虫抗原攻击后的支气管肺泡灌洗液(BAL)、外周血细胞、肺组织学检查和呼吸阻力(RRS)的研究。服用美托品的9只犬中有7只出现了左右室收缩反应，24小时内有不同程度的持续性支气管收缩(RRS：7.7±0.9cmH_2O/L/秒，243±17%初值)，显著大于对照组(P&lt；0.01)。LAR发育犬BAL液中中性粒细胞在激发后30h显著升高，BAL液中嗜酸性粒细胞显著增加，LAR组与对照组无显著差异。组织学检查显示LAR组细支气管内有明显的中性粒细胞和部分嗜酸性粒细胞的浸润。LAR组大鼠攻击后30h血清皮质醇水平明显低于对照组。我们得出的结论是：(1)内源性皮质醇可防止中性粒细胞在肺内聚集，并抑制晚期哮喘反应以及抗原攻击后持续的支气管收缩。(2)内源性皮质醇不影响嗜酸性粒细胞的聚集，嗜酸性粒细胞在LAR对抗原攻击的发展过程中可能不起重要作用。

To examine the role of inflammatory cells on the late asthmatic reaction with consequent prolonged obstructive airway changes, we studied cell profiles in bronchoalveolar lavage fluid (BAL), peripheral blood cells, histological examination of the lung and respiratory resistance (Rrs) after Ascaris suum antigen challenge in metopirone (cortisol synthesis inhibitor) treated dogs in vivo. Seven out of nine dogs treated with metopirone showed LAR, The LAR was accompanied by varying degrees of sustained bronchoconstriction over 24 hours (Rrs:7.7+0.9cmH_2O/l/sec, 243+17%initial value), which was significantly greater than control group (p<0.01). Neutrophils in BAL fluid significantly increased in LAR developed dogs 30 hours after challenge.Which eosinophils in BAL fluid increased remarkably, there was no significant difference between LAR group and control group. Histological examination revealed prominent infiltration of neutrophils and partly eosinophils in bronchioles in LAR group. Serum cortisol levels in LAR group were significantly less than control group at 30 hours after challenge. We conclude that (1) Endogenous cortisol prevents accumulation of neutrophils in the lung and inhibits late asthmatic reaction followed by prolonged bronchoconstriction after antigen challenge . (2) Endogenous cortisol does not influence accumulation of eosinophils and eosinophils may not be important in the development of LAR to antigen challenge.