Boschetto P, Zocca E, Bruchi O, Cappellazzo G, Milani G F, Pivirotto F, Mapp C E, Fabbri L M
Institute of Occupational Medicine, University of Padua, Italy.
Adv Prostaglandin Thromboxane Leukot Res. 1987;17B:1080-4.
To determine the importance of airway inflammation for late asthmatic reactions and increased airway responsiveness induced by TDI, we investigated whether late asthmatic reactions and increased responsiveness induced by TDI are associated with airway inflammation and whether steroids prevent them by modifying the inflammatory response within the airways. We measured FEV1 before and at regular intervals after exposure to TDI and performed dose-response curves to methacholine and bronchoalveolar lavage 8 hr after TDI in two subjects with previously documented late asthmatic reaction; then we repeated the same procedure a few weeks after treatment with steroids. Airway responsiveness and polymorphonuclear cells were increased in both subjects after the late asthmatic reaction; treatment with steroids prevented late asthmatic reaction and the increase in airway responsiveness and polymorphonuclear cells in bronchoalveolar lavage. These results suggest that late asthmatic reaction induced by TDI may be caused by airway inflammation.
为了确定气道炎症对由甲苯二异氰酸酯(TDI)诱发的迟发性哮喘反应及气道反应性增加的重要性,我们研究了TDI诱发的迟发性哮喘反应和反应性增加是否与气道炎症相关,以及类固醇是否通过改变气道内的炎症反应来预防这些情况。我们在两名先前记录有迟发性哮喘反应的受试者中,于接触TDI之前及之后定期测量第一秒用力呼气容积(FEV1),并在TDI接触8小时后对乙酰甲胆碱进行剂量反应曲线测定及支气管肺泡灌洗;然后在使用类固醇治疗几周后重复相同程序。两名受试者在迟发性哮喘反应后气道反应性及多形核细胞均增加;类固醇治疗预防了迟发性哮喘反应以及支气管肺泡灌洗中气道反应性和多形核细胞的增加。这些结果表明,TDI诱发的迟发性哮喘反应可能由气道炎症引起。