Ind P W, Barnes P J, Brown M J, Dollery C T
Thorax. 1985 Dec;40(12):903-9. doi: 10.1136/thx.40.12.903.
The mechanism of propranolol induced bronchoconstriction in asthma is uncertain, as airway beta adrenoceptors are not innervated by sympathetic nerves and circulating adrenaline concentrations are not raised. Propranolol 10 mg was infused over 27 minutes in 14 subjects with mild asthma. Peak expiratory flow (PEF) decreased by 80-235 l/min (17-51% of baseline) in nine subjects, who were called "responders," and by less than 50 l/min (12% of baseline) in five "non-responders". These two groups did not differ in baseline ventilatory function or in any clinical characteristic. In "responders" mean PEF had decreased significantly from 440 to 390 l/min after infusion of propranolol 2.1 mg, though the maximum fall in PEF occurred during or within five minutes of the end of the infusion. In nine of the subjects (six "responders" and three "non-responders") the possibility that propranolol induced bronchoconstriction is due to blockade of mast cell beta receptors leading to increased mediator release was examined by measurement of plasma histamine concentration as an index of mast cell degranulation. There was no consistent change in plasma histamine concentration in either group. No evidence of increased mast cell mediator release has been found in association with propranolol induced bronchoconstriction.
普萘洛尔诱发哮喘患者支气管收缩的机制尚不清楚，因为气道β肾上腺素能受体不受交感神经支配，且循环中的肾上腺素浓度也未升高。对14例轻度哮喘患者在27分钟内输注10毫克普萘洛尔。9名“反应者”的呼气峰值流速（PEF）下降了80 - 235升/分钟（为基线的17% - 51%），而5名“无反应者”的PEF下降小于50升/分钟（为基线的12%）。这两组在基线通气功能或任何临床特征方面并无差异。在“反应者”中，输注2.1毫克普萘洛尔后，平均PEF从440显著降至390升/分钟，尽管PEF的最大降幅出现在输注过程中或输注结束后五分钟内。在9名受试者（6名“反应者”和3名“无反应者”）中，通过测量血浆组胺浓度作为肥大细胞脱颗粒的指标，研究了普萘洛尔诱发支气管收缩是否是由于阻断肥大细胞β受体导致介质释放增加所致。两组的血浆组胺浓度均无一致变化。未发现与普萘洛尔诱发支气管收缩相关的肥大细胞介质释放增加的证据。
