Olsson O A, Ekdahl A
Acta Pharmacol Toxicol (Copenh). 1985 Apr;56(4):316-20. doi: 10.1111/j.1600-0773.1985.tb01296.x.
The ability of inhaled atropine and clonidine to inhibit a bronchospasm produced by injected acetylcholine or by vagal stimulation, was studied in anaesthetized guinea pigs. Vagally mediated airway constriction was restrained in a concentration-related fashion by inhaled clonidine and reached nearly 100% inhibition (EC50 = 2 X 10(-5) mol/l in the nebulizer). Atropine expressed initially about the same level of spasmolytic effect but only a final prevention of 60% was possible to reach with this drug. On the contrary, inhaled atropine was able to produce a complete inhibition (EC50 = 2 X 10(-6) mol/l) when the bronchoconstriction was elicited by exogenous acetylcholine. This type of spasm was also to some degree inhibited by clonidine.
在麻醉的豚鼠中研究了吸入性阿托品和可乐定抑制注射乙酰胆碱或迷走神经刺激所产生的支气管痉挛的能力。吸入性可乐定以浓度相关的方式抑制迷走神经介导的气道收缩，几乎达到100%抑制（雾化器中EC50 = 2×10(-5) mol/l）。阿托品最初表现出大致相同水平的解痉作用，但使用该药物最终仅能达到60%的预防效果。相反，当支气管收缩由外源性乙酰胆碱引起时，吸入性阿托品能够产生完全抑制（EC50 = 2×10(-6) mol/l）。这种类型的痉挛也在一定程度上被可乐定抑制。
