PAOLO JOSE CESARE BISELLI

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SCPACIN-62, Hospital Universitário

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Revista / Livro: European Respiratory Journal ×

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  • article 104 Citação(ões) na Scopus
    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.
  • article 54 Citação(ões) na Scopus
    Reductions in dead space ventilation with nasal high flow depend on physiological dead space volume: metabolic hood measurements during sleep in patients with COPD and controls
    (2018) BISELLI, Paolo; FRICKE, Kathrin; GROTE, Ludger; BRAUN, Andrew T.; KIRKNESS, Jason; SMITH, Philip; SCHWARTZ, Alan; SCHNEIDER, Hartmut
    Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space. 11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L center dot min(-1)) intermittently for periods of 5-10 min. We measured CO2 production and calculated dead space ventilation. Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6 +/- 0.4 to 4.8 +/- 0.4 L center dot min(-1); p< 0.05) and tidal volume (from 0.34 +/- 0.03 to 0.3 +/- 0.03 L; p< 0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5 +/- 0.4 to 1.6 +/- 0.4 L center dot min(-1); p< 0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r(2)=0.36; p< 0.05), but not with respiratory rate or anatomical dead space volume. During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.