We investigated acinar airway involvement in 20 patients with stable asthma
, using the phase III slope analysis of the multiple breath N-2 washout pre
viously applied in a group of patients with COPD (Am. J. Respir. Grit Care
Med. 1998;157:1573-1577). This technique quantifies severity of conductive
and acinar components of ventilation maldistribution separately, through in
dices S-cond and S-acin, which increase when respective ventilation inhomog
eneities increase. We also investigated the effect of salbutamol inhalation
on S-cond and S-acin in patients with asthma and compared it with that obt
ained in patients with COPD. Baseline measurements in the patients with ast
hma show that (1) acinar ventilation inhomogeneity was indeed abnormal in p
atients with asthma (S-acin = 0.195 +/- 0.026 L-1) despite the normal diffu
sing capacity in this group; S-acin values were intermediate between those
obtained in unaffected individuals and patients with COPD, and that (2) con
ductive ventilation inhomogeneity was abnormal in the patients with asthma
(S-cond = 0.076 +/- 0.006 L-1) but similar to that obtained in the patients
with COPD. Measurements after salbutamol inhalations showed significant ch
anges in S-cond and S-acin only in the patients with asthma (p < 0.001). Th
is study primarily demonstrated significant, but partially reversible, acin
ar airway impairment in patients with asthma, as compared with the more sev
ere baseline acinar airway impairment in patients with COPD, which was not
reversible after salbutamol inhalation.