Lipworth Brian J, Williamson Peter A
Asthma and Allergy Research Group, Ninewells Hospital and Medical School, University of Dundee, Dundee DD3 0QW, Scotland, UK.
Clin Sci (Lond). 2009 Oct 12;118(2):115-20. doi: 10.1042/CS20090398.
Asthma was originally thought to be associated with an intrinsic defect in beta2ADR (beta2-adrenoceptor) function, tipping the balance towards parasympathetic bronchoconstriction. Hence beta-blocking drugs (such as beta2ADR antagonists and inverse agonists) may cause acute bronchoconstriction which, in turn, may be attenuated by anti-cholinergic agents. Although beta2-agonists are highly effective for the acute relief of bronchoconstriction, their chronic use is accompanied by an adaptive reduction in beta2ADR numbers and associated desensitization of response, resulting in increased exacerbations and rare cases of death. The hypothesis examined in the present article is that, while single dosing with a beta-blocker may cause acute bronchoconstriction, chronic dosing may afford putative beneficial effects including attenuated airway hyperresponsiveness.
哮喘最初被认为与β2肾上腺素能受体（β2-ADR）功能的内在缺陷有关，使平衡倾向于副交感神经介导的支气管收缩。因此，β受体阻滞剂（如β2-ADR拮抗剂和反向激动剂）可能会导致急性支气管收缩，而抗胆碱能药物可能会减轻这种收缩。虽然β2激动剂对急性支气管收缩的缓解非常有效，但其长期使用会伴随着β2-ADR数量的适应性减少以及相关的反应脱敏，导致病情加重增加和罕见的死亡病例。本文所检验的假设是，虽然单次服用β受体阻滞剂可能会导致急性支气管收缩，但长期服用可能会产生假定的有益效果，包括减轻气道高反应性。
