Mielens E, Rosenberg F J
Br J Pharmacol. 1976 Aug;57(4):495-500. doi: 10.1111/j.1476-5381.1976.tb10376.x.
Dual effects of aspirin were demonstrated in guinea-pig lungs: (a) aspirin (3.3 mg/kg i.v.) antagonized bronchoconstriction induced by slow reacting substance of anaphylaxis (SRS-A); (b) aspirin produced bronchoconstriction when injected in the presence of propranolol into guinea-pigs in vivo at 330 mg/kg, or into guinea-pig isolated lungs in vitro as a 4% solution (40 mg/ml). 2 The severity of bronchoconstriction following administration of aspirin was directly related to the degree of beta-adrenoceptor blockade and to the age of the guinea-pigs. Aspirin-induced bronchoconstriction was prevented in vivo and in vitro by atropine and it could be reversed in vivo by atropine. Aspirin-induced bronchoconstriction was not inhibited by vagotomy or phenoxybenzamine. 3 These data suggest that the mechanism involved in aspirin-induced bronchoconstriction may be local cholinergic stimulation and that reduced beta-adrenergic drive may be a predisposing factor.
(a) 阿司匹林(静脉注射3.3毫克/千克)可拮抗过敏反应慢反应物质(SRS-A)诱导的支气管收缩;(b) 当在普萘洛尔存在的情况下,以330毫克/千克的剂量给豚鼠体内注射阿司匹林,或以4%的溶液(40毫克/毫升)给豚鼠离体肺注射时,阿司匹林会引起支气管收缩。2 服用阿司匹林后支气管收缩的严重程度与β-肾上腺素能受体阻滞程度和豚鼠年龄直接相关。阿司匹林诱导的支气管收缩在体内和体外均可被阿托品预防,且在体内可被阿托品逆转。阿司匹林诱导的支气管收缩不受迷走神经切断术或酚苄明的抑制。3 这些数据表明,阿司匹林诱导支气管收缩的机制可能是局部胆碱能刺激,而β-肾上腺素能驱动力降低可能是一个诱发因素。