PAOLO JOSE CESARE BISELLI
Projetos de Pesquisa
Unidades Organizacionais
SCPACIN-62, Hospital Universitário
19 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 19
- 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.
- Nonlinear Flow Sensor Calibration with an Accurate Syringe(2018) BISELLI, Paolo Jose Cesare; NOBREGA, Raquel Siqueira; SORIANO, Francisco GarciaFlow sensors are required for monitoring patients on mechanical ventilation and in respiratory research. Proper calibration is important for ensuring accuracy and can be done with a precision syringe. This procedure, however, becomes complex for nonlinear flow sensors, which are commonly used. The objective of the present work was to develop an algorithm to allow the calibration of nonlinear flow sensors using an accurate syringe. We first noticed that a power law equation could properly fit the pressure-flow relationship of nonlinear flow sensors. We then developed a software code to estimate the parameters for this equation using a 3 L syringe (calibration syringe). Finally, we tested the performance of a calibrated flow sensor using a different 3 L syringe (testing syringe) and a commercially available spirometer. After calibration, the sensor had a bias ranging from -1.7% to 3.0% and precision from 0.012 L to 0.039 L for volumes measured with the 3 L testing syringe. Calibrated sensor performance was at least as good as the commercial sensor. This calibration procedure can be done at the bedside for both clinical and research purposes, therefore improving the accuracy of nonlinear flow sensors.
conferenceObject Intrinsic Positive End Expiratory Pressure (peepi) Measurement In Spontaneously Breathing Patients Using Conditioned Central Venous Pressure (cvp) Signal(2016) BISELLI, P. J. C.; NOBREGA, R. S.- Nasal high-flow therapy reduces work of breathing compared with oxygen during sleep in COPD and smoking controls: a prospective observational study(2017) BISELLI, Paolo J. C.; KIRKNESS, Jason P.; GROTE, Ludger; FRICKE, Kathrin; SCHWARTZ, Alan R.; SMITH, Philip; SCHNEIDER, HartmutPatients with chronic obstructive pulmonary disease (COPD) endure excessive resistive and elastic loads leading to chronic respiratory failure. Oxygen supplementation corrects hypoxemia but is not expected to reduce mechanical loads. Nasal high-flow (NHF) therapy supports breathing by reducing dead space, but it is unclear how it affects mechanical loads of patients with COPD. The objective of this study was to compare the effects of low-flow oxygen and NHF therapy on ventilation and work of breathing (WOB) in patients with COPD and controls during sleep. Patients with COPD (n = 12) and controls (n = 6) were recruited and submitted to polysomnography to measure sleep parameters and ventilation in response to administration of oxygen and NHF. A subset of six patients also had an esophageal catheter inserted for the purpose of measuring WOB. Patients with COPD had similar minute ventilation (V-E) but lower tidal volumes than matched controls. With oxygen, SaO(2) was increased and V-E was reduced in both controls and patients with COPD, but there was an increase in transcutaneous CO2 levels. NHF produced a greater reduction in V-E and was associated with a reduction in CO2 levels. Although NHF halved WOB, oxygen produced only a minor reduction in this parameter. We conclude that oxygen produced little change in WOB, which was associated with CO2 elevations. On the other hand, NHF produced a large reduction in V-E and WOB with a concomitant decrease in CO2 levels. Our data indicate that NHF improves alveolar ventilation during sleep compared with oxygen and room air in patients with COPD and therefore can decrease their cost of breathing. NEW & NOTEWORTHY Nasal high-flow (NHF) therapy can support ventilation in patients with chronic obstructive pulmonary disease during sleep by decreasing the work of breathing and improving CO2 levels. On the other hand, oxygen supplementation corrects hypoxemia, but it produces only a minimal reduction in work of breathing and is associated with increased CO2 levels. Therefore, NHF can be a useful method to assist ventilation in patients with increased respiratory mechanical loads.
conferenceObject Baroreflex Sensitivity and Mortality in Septic dysfunction(2018) SANTOS, Fernando dos; NOGUEIRA, Antonio Carlos; BISELLI, Paolo; HOSHINO, Wagner; MOSTARDA, Cristiano Teixeira; ANGELIS, Katia De; SORIANO, Francisco Garcia; IRIGOYEN, Maria Claudia- 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.
conferenceObject - The effect of increased lung volume in chronic obstructive pulmonary disease on upper airway obstruction during sleep(2015) BISELLI, Paolo; GROSSMAN, Peter R.; KIRKNESS, Jason P.; PATIL, Susheel P.; SMITH, Philip L.; SCHWARTZ, Alan R.; SCHNEIDER, HartmutPatients with chronic obstructive pulmonary disease (COPD) exhibit increases in lung volume due to expiratory airflow limitation. Increases in lung volumes may affect upper airway patency and compensatory responses to inspiratory flow limitation (IFL) during sleep. We hypothesized that COPD patients have less collapsible airways inversely proportional to their lung volumes, and that the presence of expiratory airflow limitation limits duty cycle responses to defend ventilation in the presence of IFL. We enrolled 18 COPD patients and 18 controls, matched by age, body mass index, sex, and obstructive sleep apnea disease severity. Sleep studies, including quantitative assessment of airflow at various nasal pressure levels, were conducted to determine upper airway mechanical properties [passive critical closing pressure (Pcrit)] and for quantifying respiratory timing responses to experimentally induced IFL. COPD patients had lower passive Pcrit than their matched controls (COPD: -2.8 +/- 0.9 cmH(2)O; controls: -0.5 +/- 0.5 cmH(2)O, P = 0.03), and there was an inverse relationship of subject's functional residual capacity and passive Pcrit (-1.7 cmH(2)O/l increase in functional residual capacity, r(2) = 0.27, P = 0.002). In response to IFL, inspiratory duty cycle increased more (P = 0.03) in COPD patients (0.40 to 0.54) than in controls (0.41 to 0.51) and led to a marked reduction in expiratory time from 2.5 to 1.5 s (P < 0.01). COPD patients have a less collapsible airway and a greater, not reduced, compensatory timing response during upper airway obstruction. While these timing responses may reduce hypoventilation, it may also increase the risk for developing dynamic hyperinflation due to a marked reduction in expiratory time.
conferenceObject A New Method For Measuring Oxygen Consumption (vo2): Avoiding The Need For Flow And Oxygen Signals Synchronization(2016) NOBREGA, R. S.; BISELLI, P. J. C.- ROLE OF FOCAL ADHESION KINASE IN LUNG REMODELING OF ENDOTOXEMIC RATS(2012) PETRONI, Ricardo Costa; TEODORO, Walcy R.; GUIDO, Maria Carolina; BARBEIRO, Hermes Vieira; ABATEPAULO, Fatima; THEOBALDO, Mariana Cardillo; BISELLI, Paolo Cesare; SORIANO, Francisco GarciaDespite significant advances in the care of critically ill patients, acute lung injury continues to be a complex problem with high mortality. The present study was designed to characterize early lipopolysaccharide (LPS)-induced pulmonary injury and small interfering RNA targeting focal adhesion kinase (FAK) as a possible therapeutic tool in the septic lung remodeling process. Male Wistar rats were assigned into endotoxemic group and control group. Total collagen deposition was performed 8, 16, and 24 h after LPS injection. Focal adhesion kinase expression, interstitial and vascular collagen deposition, and pulmonary mechanics were analyzed at 24 h. Intravenous injection of small interfering RNA targeting FAK was used to silence expression of the kinase in pulmonary tissue. Focal adhesion kinase, total collagen deposition, and pulmonary mechanics showed increased in LPS group. Types I, III, and V collagen showed increase in pulmonary parenchyma, but only type V increased in vessels 24 h after LPS injection. Focal adhesion kinase silencing prevented lung remodeling in pulmonary parenchyma at 24 h. In conclusion, LPS induced a precocious and important lung remodeling. There was fibrotic response in the lung characterized by increased amount in total and specific-type collagen. These data may explain the frequent clinical presentation during sepsis of reduced lung compliance, oxygen diffusion, and pulmonary hypertension. The fact that FAK silencing was protective against lung collagen deposition underscores the therapeutic potential of FAK targeting by small interfering RNA.