Animal model of status asthmatics.

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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.