Daffonchio L, Abbracchio M P, Di Luca M, Pasargiklian R, Galli P, Hernandez A, Omini C
Institute of Pharmacological Sciences, University of Milan, Italy.
Eur Respir J Suppl. 1989 Jun;6:512s-515s.
We investigated the possible occurrence of the desensitization of pulmonary beta-receptors in a model of experimental asthma such as the ovalbumin sensitized guinea-pig. Although some differences were observed between normal and asthmatic guinea-pigs, the desensitization procedure (isoproterenol (ISO) 10(-6) M x 20 min x 2) markedly impaired the relaxing capacity of ISO, epinephrine (EPI) and procaterol. With the beta 2 agonist procaterol, the sensitized tissues seemed to be more sensitive compared to normal. In parallel, the desensitization procedure produced a greater decrease in the relaxing capacity of procaterol in the sensitized tracheas. On the other hand, the two unselective beta-agonists (ISO and EPI) did not seem to discriminate between the two experimental conditions used. These data suggest that the immunological disturbance due to the active sensitization may induce a modification in beta-adrenoceptor reactivity. The results obtained with EPI after anaphylactic challenge are in agreement with this. In fact, the relaxing capacity of EPI was markedly reduced by antigen challenge.
我们在实验性哮喘模型（如卵清蛋白致敏豚鼠）中研究了肺β受体脱敏的可能发生情况。尽管在正常豚鼠和哮喘豚鼠之间观察到了一些差异，但脱敏程序（异丙肾上腺素（ISO）10⁻⁶ M×20分钟×2次）显著损害了ISO、肾上腺素（EPI）和丙卡特罗的舒张能力。对于β₂激动剂丙卡特罗，与正常组织相比，致敏组织似乎更敏感。同时，脱敏程序使致敏气管中丙卡特罗的舒张能力下降幅度更大。另一方面，两种非选择性β激动剂（ISO和EPI）似乎并未区分所使用的两种实验条件。这些数据表明，主动致敏引起的免疫紊乱可能导致β肾上腺素能受体反应性的改变。过敏反应激发后用EPI获得的结果与此一致。事实上，抗原激发显著降低了EPI的舒张能力。
