PAOLO JOSE CESARE BISELLI
Projetos de Pesquisa
Unidades Organizacionais
SCPACIN-62, Hospital Universitário
5 resultados
Resultados de Busca
Agora exibindo 1 - 5 de 5
- 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.
- Lung Mechanics Over the Century: From Bench to Bedside and Back to Bench(2022) BISELLI, Paolo Jose Cesare; LOPES, Fernanda Degobbi Tenorio Quirino Dos Santos; RIGHETTI, Renato Fraga; MORIYA, Henrique Takachi; TIBERIO, Iolanda Ftima Lopes Calvo; MARTINS, Milton ArrudaLung physiology research advanced significantly over the last 100 years. Respiratory mechanics applied to animal models of lung disease extended the knowledge of the workings of respiratory system. In human research, a better understanding of respiratory mechanics has contributed to development of mechanical ventilators. In this review, we explore the use of respiratory mechanics in basic science to investigate asthma and chronic obstructive pulmonary disease (COPD). We also discuss the use of lung mechanics in clinical care and its role on the development of modern mechanical ventilators. Additionally, we analyse some bench-developed technologies that are not in widespread use in the present but can become part of the clinical arsenal in the future. Finally, we explore some of the difficult questions that intensive care doctors still face when managing respiratory failure. Bringing back these questions to bench can help to solve them. Interaction between basic and translational science and human subject investigation can be very rewarding, as in the conceptualization of ""Lung Protective Ventilation"" principles. We expect this interaction to expand further generating new treatments and managing strategies for patients with respiratory disease.
- 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.
- IMPACT OF TIME ON FLUID RESUSCITATION WITH HYPERTONIC SALINE (NACL 7.5%) IN RATS WITH LPS-INDUCED ACUTE LUNG INJURY(2015) PETRONI, Ricardo Costa; BISELLI, Paolo Jose Cesare; LIMA, Thais Martins de; VELASCO, Irineu Tadeu; SORIANO, Francisco GarciaAcute lung injury (ALI) is a common complication associated with septic shock that directly influences the prognosis of sepsis patients. Currently, one of the main supportive treatment modalities for septic shock is fluid resuscitation. The use of hypertonic saline (HS: 7.5% NaCl) for fluid resuscitation has been described as a promising therapy in experimental models of sepsis-induced ALI, but it has failed to produce similar results in clinical practice. Thus, we compared experimental timing versus clinical timing effectiveness (i.e., early vs. late fluid resuscitation) after the inflammatory scenario was established in a rat model of bacterial lipopolysaccharide-induced ALI. We found that late fluid resuscitation with hypertonic saline (NaCl 7.5%) did not reduce the mortality rates of animals compared with the mortality late associated with early treatment. Late fluid resuscitation with both hypertonic and normal saline increased pulmonary inflammation, decreased pulmonary function, and induced pulmonary injury by elevating metalloproteinase-2 and metalloproteinase-9 activity and collagen deposition in the animals, unlike early treatment. The animals with lipopolysaccharide-induced ALI that received late resuscitation with any kind of fluids demonstrated aggravated pulmonary injury and respiratory function. Moreover, we showed that the therapeutic window for a beneficial effect of fluid resuscitation with hypertonic saline is very narrow.
- Hypertonic Saline (NaCl 7.5 %) Reduces LPS-Induced Acute Lung Injury in Rats(2015) PETRONI, Ricardo Costa; BISELLI, Paolo Jose Cesare; LIMA, Thais Martins de; THEOBALDO, Mariana Cardillo; CALDINI, Elia Tamaso; PIMENTEL, Rosangela Nascimento; BARBEIRO, Hermes Vieira; KUBO, Suely Ariga; VELASCO, Irineu Tadeu; SORIANO, Francisco GarciaAcute respiratory distress syndrome (ARDS) is the most severe lung inflammatory manifestation and has no effective therapy nowadays. Sepsis is one of the main illnesses among ARDS causes. The use of fluid resuscitation is an important treatment for sepsis, but positive fluid balance may induce pulmonary injury. As an alternative, fluid resuscitation with hypertonic saline ((HS) NaCl 7.5 %) has been described as a promising therapeutical agent in sepsis-induced ARDS by the diminished amount of fluid necessary. Thus, we evaluated the effect of hypertonic saline in the treatment of LPS-induced ARDS. We found that hypertonic saline (NaCl 7.5 %) treatment in rat model of LPS-induced ARDS avoided pulmonary function worsening and inhibited type I collagen deposition. In addition, hypertonic saline prevented pulmonary injury by decreasing metalloproteinase 9 (MMP-9) activity in tissue. Focal adhesion kinase (FAK) activation was reduced in HS group as well as neutrophil infiltration, NOS2 expression and NO content. Our study shows that fluid resuscitation with hypertonic saline decreases the progression of LPS-induced ARDS due to inhibition of pulmonary remodeling that is observed when regular saline is used.