A novel hypothesis to explain the bronchconstrictor effect of deep inspiration in asthma

In healthy subjects deep inspiration transiently dilates the airways, while many asthmatic subjects show bronchoconstriction by a mechanism which is incompletely understood. We hypothesised that the negative intrathoracic pressure associated with deep inspiration occurring in the context of increased leakiness of the airway vasculature may temporarily increase airway oedema and thus reduce luminal diameter in subjects with asthma.

The effects of non-forced deep inspiration and forced deep inspiration through resistance (generating enhanced negative intrathoracic pressure) on specific airway conductance (sGaw) were compared in 10 asthmatic and 11 healthy subjects. Each performed two respiratory manoeuvres: (1) sGaw was measured immediately after three deep inspirations without added resistance, each performed at a predetermined rate (equal to that when performed maximally through resistance); and (2) sGaw was measured immediately after three forced inspirations through resistance.

Compared with deep inspiration without added resistance, sGaw was significantly reduced after deep inspiration through resistance in the asthmatic group by a mean (SD) of -13.5 (11.0)% (p=0.003) but was unchanged in the control group (-0.5 (12.4)%, p=0.67).

Given the similar time-volume relationship in the two manoeuvres, the reduction in sGaw is unlikely to be due to differences in smooth muscle behaviour. It is suggested that the enhanced negative intrathoracic pressure acting across the airway capillaries increases airway wall oedema and reduces airway calibre. Such a mechanism operational during normal rapid deep inspiration might contribute to bronchoconstriction after deep inspiration in subjects with asthma.