The purpose of this study was to determine whether altered airway smooth muscle (ASM) contractility contributes to the pathogenesis of obstructive airways diseases such as chronic obstructive pulmonary disease (COPD) and asthma. The passive and active mechanical properties of isolated human peripheral airways were measured in vitro by myography. The amount of ASM was measured by morphometry. Pulmonary function was assessed before surgery by the FEV(1) (%pred) and the FEV(1)/ FVC (%). Fifteen airways were studied from nonobstructed (NOB) patients, and 15 from obstructed (OB, FEV(1)/FVC < 70%) patients (62 +/- 10 yr, mean +/- SD). The maximal isometric force (Fmax), stress (Fmax/ASM), airway diameter at Lmax (Dmax), maximal isotonic shortening (%Lmax), and normalized airway smooth muscle (ASM/Dmax) were determined in all patients. There was a significant correlation between Fmax and FEV(1) (%pred) (r = -0.579, p < 0.004), between Fmax and FEV(1)/FVC (%) (r = -0.720, p < 0.003), and between stress and FEV(1)/FVC (%) (-0.611, p < 0.002). There was no correlation between isotonic shortening and either measure of pulmonary function. A positive correlation was found between force and shortening (r = 0.442, p < 0.05), and stress and shortening (r = 0.538, p < 0.01). Both force and stress were significantly increased (p < 0.05) in OB (Fmax = 0.87 +/- 0.8 g, stress = 76 +/- 47 mN/mm(2)) versus NOB (Fmax = 0.42 +/- 0.18 g, stress = 51 +/- 21 mN/mm(2)) patients, while isotonic shortening was not different between the two groups. ASM and ASM/Dmax were both significantly increased in the OB patient group (p < 0.05). These results suggest that obstructive airways disease is associated with an increase in the ability of the ASM to generate force. (Values represent means +/- SD.)