Reinhardt D, Becker B, Nagel-Hiemke M, Schiffer R, Zehmisch T
Pediatr Pharmacol (New York). 1983;3(3-4):293-302.
The most attractive "adrenergic theory" has proposed that in asthmatic patients the bronchial hyperreactivity might be caused by a decreased beta-receptor and an increased alpha-receptor responsiveness. Based upon the assumption that an abnormality of adrenergic receptors might be a general phenomenon, we have performed receptor-binding studies on lymphocytes and thrombocytes from asthmatic children who had and had not undergone treatment with beta-receptor agonists and/or glucocorticoids. Iodo-cyano-pindolol and tritium-labeled yohimbine were used as beta- and alpha-receptor ligands. The following results have been obtained: 1) The number and affinity of alpha- and beta-adrenoceptors on thrombocytes and lymphocytes showed no significant differences in asthmatic children and their age-matched controls. 2) In vivo treatment of asthmatic children with beta-receptor agonists immediately reduced the number of beta-receptors ("down regulation"). A reversal of the number of beta-receptors occurred within 1 day after cessation of the therapy. Although it appeared that some asthmatics with severe asthma have a reduced number of beta-receptors, in vivo treatment with beta-receptor agonists thus might mimic a beta-receptor blockade. 3) High-dose treatment with glucocorticoids increased the number of beta-receptors but left the alpha-receptors unaffected.
最具吸引力的“肾上腺素能理论”提出，哮喘患者的支气管高反应性可能是由β受体减少和α受体反应性增加所致。基于肾上腺素能受体异常可能是一种普遍现象这一假设，我们对接受和未接受β受体激动剂和/或糖皮质激素治疗的哮喘儿童的淋巴细胞和血小板进行了受体结合研究。碘氰吲哚洛尔和氚标记的育亨宾分别用作β和α受体配体。获得了以下结果：1）哮喘儿童及其年龄匹配的对照组血小板和淋巴细胞上α和β肾上腺素能受体的数量和亲和力无显著差异。2） 用β受体激动剂对哮喘儿童进行体内治疗可立即减少β受体数量（“下调”）。治疗停止后1天内β受体数量出现逆转。虽然似乎一些重度哮喘患者的β受体数量减少，但用β受体激动剂进行体内治疗可能会模拟β受体阻断。3） 大剂量糖皮质激素治疗可增加β受体数量，但α受体不受影响。
