Background: This study was conducted in order to investigate the differences in the respiratory physiology of patients with chronic obstructive pulmonary disease (COPD), asthma-COPD overlap syndrome (ACOS), and asthma with airflow limitation (asthma FL⁺). Methods: The medical records for a series of all stable patients with persistent airflow limitation due to COPD, ACOS, or asthma were retrospectively reviewed and divided into the COPD group (n=118), the ACOS group (n=32), and the asthma FL⁺ group (n=27). All the patients underwent chest high-resolution computed tomography (HRCT) and pulmonary function tests, including respiratory impedance. Results: The low attenuation area score on chest HRCT was significantly higher in the COPD group than in the ACOS group (9.52±0.76 vs 5.09±1.16, P<0.01). The prevalence of bronchial wall thickening on chest HRCT was significantly higher in the asthma FL⁺ group than in the COPD group (55.6% vs 25.0%, P<0.01). In pulmonary function, forced expiratory volume in 1 second (FEV₁) and peak expiratory flow rate were significantly higher in the asthma FL⁺ group than in the ACOS group (76.28%±2.54% predicted vs 63.43%±3.22% predicted, P<0.05 and 74.40%±3.16% predicted vs 61.08%±3.54% predicted, P<0.05, respectively). Although residual volume was significantly lower in the asthma FL⁺ group than in the COPD group (112.05%±4.34% predicted vs 137.38%±3.43% predicted, P<0.01) and the ACOS group (112.05%±4.34% predicted vs148.46%±6.25% predicted, P<0.01), there were no significant differences in functional residual capacity or total lung capacity. The increase in FEV₁ in response to short-acting ß₂-agonists was significantly greater in the ACOS group than in the COPD group (229±29 mL vs 72±10 mL, P<0.01) and the asthma FL⁺ group (229±29 mL vs 153±21 mL, P<0.05). Regarding respiratory impedance, resistance at 5 Hz and resistance at 20 Hz, which are oscillatory parameters of respiratory resistance, were significantly higher in the asthma FL⁺ group than in the COPD group at the whole-breath (4.29±0.30 cmH₂O/L/s vs 3.41±0.14 cmH₂O/L/s, P<0.01 and 3.50±0.24 cmH₂O/L/s vs 2.68±0.10 cmH₂O/L/s, P<0.01, respectively), expiratory, and inspiratory phases. Conclusion: Although persistent airflow limitation occurs in patients with COPD, ACOS, and asthma FL⁺, they may have distinct characteristics of the respiratory physiology and different responsiveness to bronchodilators.

The present study was performed to examine the occurrence of dynamic hyperinflation following hyperventilation in COPD patients and former smokers without COPD, and the efficacy of short-acting anticholinergic agents (SAAC) and beta2-agonists (SABA) for lung hyperinflation following metronome-paced hyperventilation in COPD. Fifty-nine patients with COPD, 20 ex-smokers without COPD and 20 healthy subjects who had never smoked were examined for dynamic hyperinflation by metronome-paced hyperventilation with respiratory rate increasing from 20 to 30 and 40 tidal breaths/min. Dynamic hyperinflation was evaluated as the decrease in inspiratory capacity (IC) following hyperventilation, and the effects of SAAC and SABA on dynamic hyperinflation were assessed. COPD patients showed a significant increase in end-expiratory lung volume and a decrease in IC following hyperventilation, and ex-smokers without COPD also showed mild but significant dynamic hyperinflation. Multiple stepwise linear regression analysis revealed that the carbon monoxide transfer coefficient (DLco/VA) and RV/TLC were significant and independent determinants of dynamic hyperinflation in COPD. Treatment with SAAC and SABA significantly increased IC at each respiratory rate, independently of the increases in FEV1. Furthermore, SABA significantly inhibited the decrease in IC due to hyperventilation. These findings suggest that lung hyperinflation following hyperventilation may be a useful method for detecting dynamic hyperinflation observed not only in patients with COPD but also in ex-smokers without COPD, and both SAAC and SABA are effective in reducing dynamic hyperinflation in COPD.

Purpose: Cigarette smoke produces a high level of acrolein, which is thought to be pathogenically involved in the development of chronic obstructive pulmonary disease (COPD). The present study investigated the pathological role of acrolein in the development of COPD. Patients and methods: Acrolein concentration was measured in plasmas obtained from 47 patients with COPD and 18 current smokers without COPD, and in supernatants of homogenized lung tissues obtained from 10 never-smokers, 8 current smokers, and 8 patients with COPD by high-performance liquid chromatography. Oxidant status and antioxidant activity were measured using derivatives of reactive oxygen metabolite (d-ROM) and bio-antioxidant power (BAP), respectively, in the Free Radical Elective Evaluation FRAS4 system. In addition, immunohistochemistry was used to evaluate the over-presentation of acrolein in lung tissues of patients with COPD. Results: Plasma concentrations of acrolein were significantly higher in the patients with COPD than the non-COPD smokers (P<0.001), which significantly correlated with the oxidant status in patients with COPD (R=0.69, P<0.05). Similar pathological alterations in acrolein concentrations were found in the lung tissue supernatants of patients with COPD, which significantly correlated with the oxidant status in patients with COPD. Furthermore, acrolein was strongly expressed in the lung tissues of patients with COPD. Conclusion: The increased acrolein concentrations were highly involved in the pathogenesis of COPD through interference in the balance of oxidative stress versus antioxidant potentiality.