Sympathetic activation and parasympathetic withdrawal are commonly observed during acute exacerbations of chronic obstructive pulmonary disease (COPD). We have demonstrated previously that noninvasive positive-pressure ventilation (NPPV) improves parasympathetic neural control of heart rate in patients with obstructive sleep apnea. We hypothesized that NPPV may exert such beneficial effects in COPD as well. Therefore, we assessed the acute effects of NPPV on systemic blood pressure and indexes of heart rate variability (HRV) in 23 patients with acute exacerbations of COPD. The measurements of HRV in the frequency domain were computed by an autoregressive spectral technique. The use of NPPV resulted in significant increases of oxygen saturation (from 89.2±1.0 to 92.4±0.9 %, p<0.001) in association with reductions in systolic and diastolic blood pressures and heart rate (from 147±3 to 138±3 mm Hg, from 86±2 to 81±2 mm Hg, from 85±3 to 75±2 bpm, p<0.001 for all variables), and increases in ln-transformed high frequency band of HRV (from 6.4±0.5 to 7.4±0.6 ms2/Hz, p<0.01). Reductions in heart rate and increases in ln-transformed HF band persisted after NP PV withdrawal. In conclusion, these findings suggest that NPPV may cause improvements in the neural control of heart rate in patients with acute exacerbations of COPD., P. Skyba, P. Joppa, M. Orolín, R. Tkáčová., and Obsahuje bibliografii a bibliografické odkazy
Increases in resting energy expenditure (REE) likely contribute to weight loss in various chronic diseases. In chronic obstructive pulmonary disease (COPD), relationships between the ventilatory impairment and increased REE, and between disturbances in adipokines and weight loss were previously described. Therefore, we investigated serum levels and adipose tissue expression of leptin and adiponectin, and their relationships to REE in patients with COPD. In 44 patients with stable COPD (38 male; age 62.3±7.2 years), REE was assessed using indirect calorimetry. Subcutaneous adipose tissue samples were analyzed using realtime PCR. From underweight [n=9; body mass index (BMI) <20.0 kg.m−2 ], to normal weight-overweight (n=24, BMI=20.0- 29.9 kg.m−2 ) and obese patients (n=11; BMI≥30 kg.m−2 ), REE adjusted for body weight decreased (32.9±6.1 vs. 26.2±5.8 vs. 23.9±6.6 kcal.kg−1 .24 h−1 , p=0.006), serum levels and adipose tissue expression of leptin increased (p<0.001 for both), and serum and adipose tissue adiponectin decreased (p<0.001; p=0.004, respectively). REE was inversely related to serum and adipose tissue leptin (R=−0.547, p<0.001; R=−0.458, p=0.002), and directly to serum adiponectin (R=0.316, p=0.039). Underweight patients had increased REE compared to normal weight-overweight patients, in association with reductions in serum and adipose tissue leptin, and increased serum adiponectin, suggesting a role of adipokines in energy imbalance in COPD-related cachexia, M. Brúsik ... [et al.]., and Obsahuje seznam literatury
Proteasomes appear to be involved in the pathophysiology of various acute and chronic lung diseases. Information on the human lung proteasome in health and disease, however, is sparse. Therefore, we studied whether end-stage pulmonary diseases are associated with alterations in lung 20S/26S proteasome content, activity and 20S subunit composition. Biopsies were obtained from donor lungs (n=7) and explanted lungs from patients undergoing lung transplantation because of end stage chronic obstructive pulmonary disease (COPD; n=7), idiopathic pulmonary fibrosis (IPF, n=7) and pulmonary sarcoidosis (n=5). 20S/26S proteasomes in lung extracts were quantified by ELISA, chymotrypsin-like proteasome peptidase activities measured and 20S proteasome β subunits analyzed by Western blot. As compared with donor lungs, proteasome content was increased in IPF and sarcoidosis, but not in COPD. The relative distribution of free 20S and 26S proteasomes was similar; 20S proteasome was predominant in all extracts. Proteasome peptidase activities in donor and diseased lungs were indistinguishable. All extracts contained a mixed composition of inducible 20S β immuno-subunits and their constitutive counterparts; a disease associated distribution could not be identified. A higher content of lung proteasomes in IPF and pulmonary sarcoidosis may contribute to the pathophysiology of human fibrotic lung diseases., T. A. Baker, H. H. Bach IV, R. L. Gemelli, R. B. Love, M. Majetschak., and Obsahuje bibliografii
Chronic obstructive pulmonary disease (COPD) is a progressive and disabling disease that has been associated with aging. Several factors may potentially impair performance during exercise in elderly patients with COPD. This study was conducted to evaluate what characteristics related to lung function, peripheral muscle strength and endurance can predict the performance of elderly patients with COPD during cardiopulmonary exercise testing (CPET). Forty elderly patients with COPD underwent resting lung function tests, knee isokinetic dynamometry, and CPET. Three models were developed to explain the variability in peak oxygen uptake (VO2 peak) after controlling for age as an independent confounder. The pulmonary function model showed the highest explained variance (65.6 %); in this model, ventilation distribution (p<0.001) and pulmonary diffusion (0.013) were found to be independent predictors. Finally, the models that included the muscle strength and endurance variables presented explained variances of 51 % and 57.4 %, respectively. In these models that involved muscular dysfunction, however, only the endurance variables were found to be independent predictors (p<0.05). In conclusion, ventilation distribution and pulmonary diffusion, but not the degree of airway obstruction, independently predict CPET performance in elderly patients with COPD. In addition, peripheral muscle endurance, but not strength, also predicts CPET performance in these subjects.