Peripheral airway smooth muscle mechanics in obstructive airways disease

The purpose of this study was to determine whether altered airway smooth mu scle (ASM) contractility contributes to the pathogenesis of obstructive air ways diseases such as chronic obstructive pulmonary disease (COPD) and asth ma. The passive and active mechanical properties of isolated human peripher al airways were measured in vitro by myography. The amount of ASM was measu red by morphometry. Pulmonary function was assessed before surgery by the F EV1 (%pred) and the FEV1/FVC (%). Fifteen airways were studied from nonobst ructed (NOB) patients, and 15 from obstructed (OB, FEV1/FVC < 70%) patients (62 +/- 10 yr, mean +/- SD). The maximal isometric force (Fmax), stress (F max/ASM), airway diameter at Lmax (Dmax), maximal isotonic shortening (%Lma x), and normalized airway smooth muscle (ASM/Dmax) were determined in all p atients, There was a significant correlation between Fmax and FEV1 (%pred) (r = -0.579, p < 0.004), between Fmax and FEV1/FVC (%) (r = -0.720, p < 0.0 03), and between stress and FEV1/FVC (%) (-0.611, p < 0.002). There was no correlation between isotonic shortening and either measure of pulmonary fun ction. 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, str ess = 51 +/- 21 mN/mm(2)) patients, while isotonic shortening was not diffe rent between the two groups. ASM and ASM/Dmax were both significantly incre ased in the OB patient group (p < 0.05). These results suggest that obstruc tive airways disease is associated with an increase in the ability of the A SM to generate force. (Values represent means +/- SD.).