PAOLO JOSE CESARE BISELLI
Projetos de Pesquisa
Unidades Organizacionais
SCPACIN-62, Hospital Universitário
3 resultados
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- 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.
- 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.
- Leptin and the control of pharyngeal patency during sleep in severe obesity(2014) SHAPIRO, Steven D.; CHIN, Chien-Hung; KIRKNESS, Jason P.; MCGINLEY, Brian M.; PATIL, Susheel P.; POLOTSKY, Vsevolod Y.; BISELLI, Paolo Jose Cesare; SMITH, Philip L.; SCHNEIDER, Hartmut; SCHWARTZ, Alan R.Rationale: Obesity imposes mechanical loads on the upper airway, resulting in flow limitation and obstructive sleep apnea (OSA). In previous animal models, leptin has been considered to serve as a stimulant of ventilation and may prevent respiratory depression during sleep. We hypothesized that variations in leptin concentration among similarly obese individuals will predict differences in compensatory responses to upper airway obstruction during sleep. Methods: An observational study was conducted in 23 obese women [body mass index (BMI): 46 +/- 3 kg/m(2), age: 41 +/- 12 yr] and 3 obese men (BMI: 46 +/- 3 kg/m(2), age: 43 +/- 4 yr). Subjects who were candidates for bariatric surgery were recruited to determine upper airway collapsibility under hypotonic conditions [pharyngeal critical pressure (passive PCRIT)], active neuromuscular responses to upper airway obstruction during sleep, and overnight fasting serum leptin levels. Compensatory responses were defined as the differences in peak inspiratory airflow (Delta V(I)max), inspired minute ventilation (Delta V-I), and pharyngeal critical pressure (Delta P-CRIT) between the active and passive conditions. Results: Leptin concentration was not associated with sleep disordered breathing severity, passive P-CRIT, or baseline ventilation. In the women, increases in serum leptin concentrations were significantly associated with increases in Delta V(I)max (r(2) = 0.44, P < 0.001), Delta V-I (r(2) = 0.40, P < 0.001), and Delta P-CRIT (r(2) = 0.19, P < 0.04). These responses were independent of BMI, waist-to-hip ratio, neck circumference, or sagittal girth. Conclusion: Leptin may augment neural compensatory mechanisms in response to upper airway obstruction, minimizing upper airway collapse, and/or mitigating potential OSA severity. Variability in leptin concentration among similarly obese individuals may contribute to differences in OSA susceptibility.