Abstract

There is uncertainty about the relative contributions of bronchial smooth muscle contraction, mucosal oedema and mucus plugging to airflow obstruction in the allergen-induced late asthmatic response (LAR). We systematically studied the ability of the inhaled beta 2-agonist salbutamol to reverse the LAR in eight subjects after allergen bronchoprovocation. Salbutamol reversed the LAR by restoring FEV1 to a level similar to the initial value measured at the same time of day (18.00 h) on the previous evening. For the eight subjects studied, this initial FEV1 value, measured after abstaining from beta-agonists for 8 h, was a mean +/- SEM 90.7 +/- 5.6% of predicted, which suggests further bronchodilation may have been possible at this time. We then studied six of the eight subjects in an identical protocol with saline challenge substituted for allergen bronchoprovocation to answer the question whether further bronchodilation was possible at that time after salbutamol in the absence of an LAR. After salbutamol on the allergen challenge day the FEV1 for the six subjects was 84.1 +/- 7.0% of predicted, compared with 94.0 +/- 3.7% of predicted at the same point on the saline challenge day (P < 0.05). We conclude that, although the LAR may be effectively reversed by beta 2-agonists, there is evidence for some residual airway narrowing, presumably related to mucosal oedema, exudate and mucus plugging.

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