Airway closure with methacholine-induced bronchoconstriction.

We examined airway closure with methacholine-induced bronchoconstriction in eight normal seated adults at a mean lung volume of 39% total lung capacity. Closure was evaluated in two ways. Regional closure was examined by comparing the regional distributions of 133Xe boluses distributed according to N2O uptake with those distributed by pulmonary perfusion; regions that exhibited less N2O uptake than perfusion were interpreted as having airway closure. In addition, we measured single-breath washouts of the same boluses; differences between the washouts indicated closure that was not necessarily regional. Basal airway closure increased with methacholine inhalation from 21 +/- 3 to 46 +/- 4% (means +/- SE; P less than 0.001). This was due to both decreased basal N2O uptake and a relative increase of basal perfusion. Washout curves of boluses distributed by perfusion did not change with bronchoconstriction. Before bronchoconstriction, washouts of boluses distributed by N2O uptake did not differ significantly from those distributed by perfusion. During bronchoconstriction, single-breath washouts of boluses distributed by N2O uptake showed increased concentration differences (P less than 0.015) that were significantly greater than those resulting from boluses delivered by perfusion. Changes in basal closure did not correlate with washout changes. We conclude that methacholine inhalation induced bronchoconstriction-increased basal airway closure and also increased airway closure in other lung regions in a way that did not relate to basal closure.