Abstract

Induced bronchoconstriction in normal subjects can be transiently reversed by a deep breath (airway hysteresis). The mechanisms of airway hysteresis are not fully understood. The aim of these studies was to determine whether the nature of the deep breath (slow or fast inspiration, five or 10 second breath hold) affects the resultant bronchodilatation. Bronchoconstriction was induced in 10 normal subjects by inhalation of histamine until specific airway conductance (sGaw) was halved (mean (SEM) post-histamine sGaw 0.099* (0.009) s-1 cm H2O-1). A subsequent deep breath to total lung capacity (TLC) increased sGaw by 57% (13%) and neither the rate of inspiration to TLC nor periods of breath holding at TLC produced a significantly different degree of bronchodilation. Reducing the volume of the deep breath produced progressively less bronchodilatation and this was no longer significant after a breath to 68% (2%) TLC. To determine whether the volume of the deep breath or the accompanying increase in transpulmonary pressure (PstL) was responsible for the effect on sGaw, subjects were studied with an oesophageal balloon in place with and without their chest strapped. Subjects took a deep breath to a PstL of 20 cm H2O after bronchoconstriction had been induced by histamine. The degree of bronchodilatation (mean (SEM) %) was not significantly different (strap on 25 (6), strap off 36 (5)) even though significantly larger lung volumes (as % TLC) were reached with the strap off (strap on 57 (2), strap off 78 (3)). These results suggest that PstL rather than lung volume during a deep breath determines airway hysteresis.