Fabbri L M, Di Giacomo R, Dal Vecchio L, Zocca E, De Marzo N, Maestrelli P, Mapp C E
Bull Eur Physiopathol Respir. 1985 Sep-Oct;21(5):421-6.
We investigated whether late asthmatic reactions and the associated increase in airway responsiveness induced by toluene diisocyanate (TDI) in sensitized subjects are inhibited by indomethacin and/or prednisone. Four sets of experiments were conducted in five subjects sensitized to TDI. To assess late asthmatic reactions to TDI, FEV1 was measured immediately before and after exposure to TDI and then hourly for 8 h. To assess change in airway responsiveness, the provocative dose (mg) of methacholine that caused a decrease in FEV1 of 20% (PD20FEV1) before treatment, and then before and after exposure to TDI was measured. In the first set of experiments, each subject was given no treatment and was studied before and 8 h after exposure to TDI; in the other two sets, each subject was studied before treatment, then during treatment with indomethacin (50 mg q.i.d. for 3 days, orally) or prednisone (50 mg once a day, for 3 days, orally), both before and 8 h after TDI exposure. In a fourth series of experiments, each subject was again given no treatment and studied before and 8 h after TDI. When the subjects were given no treatment or indomethacin, TDI caused late asthmatic reactions and increased airway responsiveness to inhaled methacholine. In contrast, when the subjects were given prednisone, TDI caused neither late asthmatic reactions nor increased airway responsiveness. Treatment with indomethacin and prednisone did not change baseline FEV1 and airway responsiveness. These results suggest that release of prostaglandins does not contribute to late asthmatic reactions and the associated increase in airway responsiveness induced by TDI. Inflammatory mediators inhibited by prednisone but not by indomethacin may be involved.
我们研究了消炎痛和/或强的松是否能抑制致敏个体中由甲苯二异氰酸酯（TDI）诱发的迟发性哮喘反应以及相关的气道反应性增加。对5名对TDI致敏的受试者进行了4组实验。为评估对TDI的迟发性哮喘反应，在接触TDI之前和之后立即测量第一秒用力呼气量（FEV1），然后每小时测量1次，共8小时。为评估气道反应性的变化，测量治疗前、接触TDI之前和之后引起FEV1下降20%的乙酰甲胆碱激发剂量（mg）（PD20FEV1）。在第一组实验中，每位受试者不接受治疗，在接触TDI之前和之后8小时进行研究；在另外两组实验中，每位受试者在治疗前、然后在使用消炎痛（50mg，每日4次，口服，共3天）或强的松（50mg，每日1次，口服，共3天）治疗期间、接触TDI之前和之后8小时进行研究。在第四组实验中，每位受试者再次不接受治疗，在接触TDI之前和之后8小时进行研究。当受试者不接受治疗或使用消炎痛时，TDI引起迟发性哮喘反应并增加对吸入乙酰甲胆碱的气道反应性。相比之下，当受试者使用强的松时，TDI既不引起迟发性哮喘反应，也不增加气道反应性。使用消炎痛和强的松治疗并未改变基线FEV1和气道反应性。这些结果表明，前列腺素的释放对TDI诱发的迟发性哮喘反应和相关的气道反应性增加没有作用。可能涉及到受强的松而非消炎痛抑制的炎症介质。
