PAOLO JOSE CESARE BISELLI
Projetos de Pesquisa
Unidades Organizacionais
SCPACIN-62, Hospital Universitário
2 resultados
Resultados de Busca
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- Aerobic exercise attenuates pulmonary injury induced by exposure to cigarette smoke(2012) TOLEDO, A. C.; MAGALHAES, R. M.; HIZUME, D. C.; VIEIRA, R. P.; BISELLI, P. J. C.; MORIYA, H. T.; MAUAD, T.; LOPES, F. D. T. Q. S.; MARTINS, M. A.It has recently been suggested that regular exercise reduces lung function decline and risk of chronic obstructive pulmonary disease (COPD) among active smokers; however, the mechanisms involved in this effect remain poorly understood. The present study evaluated the effects of regular exercise training in an experimental mouse model of chronic cigarette smoke exposure. Male C57BL/6 mice were divided into four groups (control, exercise, smoke and smoke+exercise). For 24 weeks, we measured respiratory mechanics, mean linear intercept, inflammatory cells and reactive oxygen species (ROS) in bronchoalveolar lavage (BAL) fluid, collagen deposition in alveolar walls, and the expression of antioxidant enzymes, matrix metalloproteinase 9, tissue inhibitor of metalloproteinase (TIMP) 1, interleukin (IL)-10 and 8-isoprostane in alveolar walls. Exercise attenuated the decrease in pulmonary elastance (p<0.01) and the increase in mean linear intercept (p=0.003) induced by cigarette smoke exposure. Exercise substantially inhibited the increase in ROS in BAL fluid and 8-isoprostane expression in lung tissue induced by cigarette smoke. In addition, exercise significantly inhibited the decreases in IL-10, TIMP1 and CuZn superoxide dismutase induced by exposure to cigarette smoke. Exercise also increased the number of cells expressing glutathione peroxidase. Our results suggest that regular aerobic physical training of moderate intensity attenuates the development of pulmonary disease induced by cigarette smoke exposure.
- Nasal high flow, but not supplemental O-2, reduces peripheral vascular sympathetic activity during sleep in COPD patients(2018) FRICKE, K.; SCHNEIDER, H.; BISELLI, P.; HANSEL, N. N.; ZHANG, Z. G.; SOWHO, M. O.; GROTE, L.Introduction: Patients with COPD have increased respiratory loads and altered blood gases, both of which affect vascular function and sympathetic activity. Sleep, particularly rapid eye movement (REM) sleep, is known to exacerbate hypoxia and respiratory loads. Therefore, we hypothesize that nasal high flow (NHF), which lowers ventilatory loads, reduces sympathetic activity during sleep and that this effect depends on COPD severity. Methods: We performed full polysomnography in COPD patients (n=17; FEV1, 1.6 +/- 0.6 L) and in matched controls (n=8). Participants received room air (RA) at baseline and single night treatment with O-2 (2 L/min) and NHF (20 L/min) in a random order. Finger pulse wave amplitude (PWA), a measure of vascular sympathetic tone, was assessed by photoplethysmography. Autonomic activation (AA) events were defined as PWA attenuation >= 30% and indexed per hour for sleep stages (AA index [AAI]) at RA, NHF, and O-2). Results: In COPD, sleep apnea improved following O-2 (REM-apnea hypopnea index [AHI] with RA, O-2, and NHF: 18.6 +/- 20.9, 12.7 +/- 18.1, and 14.4 +/- 19.8, respectively; P=0.04 for O-2 and P=0.06 for NHF). REM-AAI was reduced only following NHF in COPD patients (AAI-RA, 21.5 +/- 18.4 n/h and AAI-NHF, 9.9 +/- 6.8 n/h, P=0.02) without changes following O-2 (NFIF-O-2 difference, P=0.01). REM-AAI reduction was associated with lung function expressed as FEV1 and FVC (FEV1: r=-0.59, P=0.001; FEV1/FVC: r=-0.52 and P=0.007). Conclusion: NHF but not elevated oxygenation reduces peripheral vascular sympathetic activity in COPD patients during REM sleep. Sympathetic off-loading by NHF, possibly related to improved breathing mechanics, showed a strong association with COPD severity.