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

Airway constriction during a breath hold could not be examined previou sly using standard methods. We used high-resolution computed tomograph y (HRCT) in vivo to assess the temporal changes in airway area and the effects of a deep inspiration with and without vagal suppression. Fiv e dogs were anesthetized, intubated, and their lungs ventilated with 1 00 percent oxygen. Fifteen HRCT slices were obtained at functional res idual capacity (FPC) either immediately after stopping ventilation at end expiration after either a tidal volume breath or three deep inspir ations. Subsequently the dogs were given atropine, 0.2 mg/kg, and the scans were repeated. The cross-sectional areas of 33 airways ranging i n size from 1.6 to 9.7 mm in diameter were measured. Airways were sepa rated 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, me dium, 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 a n initial dilation only in the smallest airways to 133.3+/-4 percent. The subsequent constrictions were even greater than after the tidal vo lume breath averaging 67+/-15 percent, 61+/-6 percent, and 60+/-9 perc ent of initial airway area in the small, medium, and large airways, re spectively (p=0.001). Atropine caused an average increase in baseline airway area of 115+/-5 percent and 121+/-6 percent after a tidal volum e breath and deep inspiration, respectively, compared with the preatro pine controls, with no difference between the three groups. Atropine a lso 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 expirat ory pause, and a deep inspiration significantly augments this airway c onstriction. These responses are mediated via vagal afferent pathways, likely arising from progressively decreasing slow-adapting receptor ac tivity.