Endothelin -I (ET-I) is a potent brodchoconstrictor which may have a role in the pathogenesis of asthma. To thrill, the interrelation between ET-1 and bronchial asthma, the concentrations of the ET-1 in the sera and BAL fluid were measured in (JO) healthy subjects, (10) patients with atopic asthma treated with bronchodilators alone (Group I), and (10) patients with atopic asthma treated with inhaled and / .or oral corticosteroids (Group II). Pulmonary functions (FEVI% predicted and FEF2545% predicated) and the provocation concentrations of methacholine required to reduce FEVI by 20% of the prechallenge baseline (PD20) were also measured. There was no significant difference in the plasma ET-1 level among either the control group and group I (15.95 ±6.5pg/nd versus 17.84 ± 7.8 pghtd) and group II (15.95 ± 6.5 pent! versus 16.75 _± 6.7 pent!) or group land It (17.84 ± 7.8 versus 16.75 ± 6.7 pg/m1). There was a significant increase in ML fluid ET-I levels in both the non steroid treated patients with asthma(Group I) and the steroid treated patients (Group II) compared with the normal subjects (20.94 ± 3.96 pg/m1 versus 15.61 ± 3.37 pghtd) and (16.03 3.5pg/m1 versus 15.61 ±3.37 pend) respectively. There was, statistically significant difference in BAL ET-I level between Group II and group 1 indicating that ET-I BAL level may be modulated by corticosteroid therapy. In group I and II there was a significant negative correlation between the BAL ET-1 concentrations and ventilatory functions (% predicated FEVI and FET2545). No correlation between BAL fluid ET-1 concentrations and bronchial reactivity or plasma ET-I level was found in either Group 1 and II. These findings indicate that the potent bronchoconstrictive substance, endotheline, may contribute to the patho |
