SPONTANEOUS AIRWAYS CONSTRICT DURING BREATH-HOLDING STUDIED BY HIGH-RESOLUTION COMPUTED-TOMOGRAPHY

Airway constriction during a breath hold could not be examined previously using standard methods. We used high-resolution computed tomography (HRCT) in vivo to assess the temporal changes in airway area and the effects of a deep inspiration with and without vagal suppression. Five dogs were anesthetized, intubated, and their lungs ventilated with 100 percent oxygen. Fifteen HRCT slices were obtained at functional residual capacity (FPC) either immediately after stopping ventilation at end expiration after either a tidal volume breath or three deep inspirations. Subsequently the dogs were given atropine, 0.2 mg/kg, and the scans were repeated. The cross-sectional areas of 33 airways ranging in size from 1.6 to 9.7 mm in diameter were measured. Airways were separated in three groups based on size: small (<3 mm in diameter); medium (3 to 6-mm in diameter); and large (>6 mm in diameter). The small, medium, and large airways showed a spontaneous constriction over time to 49+/-8 percent, 83+/-4 percent, and 82+/-4 percent of initial airway-size, respectively (p<0.01), (p<0.0001). The deep inspiration caused an initial dilation only in the smallest airways to 133.3+/-4 percent. The subsequent constrictions were even greater than after the tidal volume breath averaging 67+/-15 percent, 61+/-6 percent, and 60+/-9 percent of initial airway area in the small, medium, and large airways, respectively (p=0.001). Atropine caused an average increase in baseline airway area of 115+/-5 percent and 121+/-6 percent after a tidal volume breath and deep inspiration, respectively, compared with the preatropine controls, with no difference between the three groups. Atropine also completely abolished the spontaneous airway constriction observed after either a tidal volume breath or a deep inspiration in all three groups equally. In conclusion, using direct airway imaging in vivo, we found that airways spontaneously constrict during a prolonged expiratory pause, and a deep inspiration significantly augments this airway constriction. These responses are mediated via vagal afferent pathways,likely arising from progressively decreasing slow-adapting receptor activity.