JOAO BATISTA BORGES SOBRINHO DORINI
Projetos de Pesquisa
Unidades Organizacionais
LIM/09 - Laboratório de Pneumologia, Hospital das Clínicas, Faculdade de Medicina
3 resultados
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- Hyperoxia affects the regional pulmonary ventilation/perfusion ratio: an electrical impedance tomography study(2014) LI, Y.; TESSELAAR, E.; BORGES, J. B.; BOHM, S. H.; SJOBERG, F.; JANEROT-SJOBERG, B.Background The way in which hyperoxia affects pulmonary ventilation and perfusion is not fully understood. We investigated how an increase in oxygen partial pressure in healthy young volunteers affects pulmonary ventilation and perfusion measured by thoracic electrical impedance tomography (EIT). Methods Twelve semi-supine healthy male volunteers aged 21-36 years were studied while breathing room air and air-oxygen mixtures (FiO2) that resulted in predetermined transcutaneous oxygen partial pressures (tcPO2) of 20, 40 and 60kPa. The magnitude of ventilation (Zv) and perfusion (ZQ)-related changes in cyclic impedance variations, were determined using an EIT prototype equipped with 32 electrodes around the thorax. Regional changes in ventral and dorsal right lung ventilation (V) and perfusion (Q) were estimated, and V/Q ratios calculated. Results There were no significant changes in Zv with increasing tcPO2 levels. ZQ in the dorsal lung increased with increasing tcPO2 (P=0.01), whereas no such change was seen in the ventral lung. There was a simultaneous decrease in V/Q ratio in the dorsal region during hyperoxia (P=0.04). Two subjects did not reach a tcPO2 of 60kPa despite breathing 100% oxygen. Conclusion These results indicate that breathing increased concentrations of oxygen induces pulmonary vasodilatation in the dorsal lung even at small increases in FiO2. Ventilation remains unchanged. Local mismatch of ventilation and perfusion occurs in young healthy men, and the change in ventilation/perfusion ratio can be determined non-invasively by EIT.
- Early Inflammation Mainly Affects Normally and Poorly Aerated Lung in Experimental Ventilator-Induced Lung Injury*(2014) BORGES, Joao Batista; COSTA, Eduardo L. V.; SUAREZ-SIPMANN, Fernando; WIDSTROM, Charles; LARSSON, Anders; AMATO, Marcelo; HEDENSTIERNA, GoranObjective: The common denominator in most forms of ventilator-induced lung injury is an intense inflammatory response mediated by neutrophils. PET with [F-18]fluoro-2-deoxy-d-glucose can be used to image cellular metabolism, which, during lung inflammatory processes, mainly reflects neutrophil activity, allowing the study of regional lung inflammation in vivo. The aim of this study was to assess the location and magnitude of lung inflammation using PET imaging of [F-18]fluoro-2-deoxy-d-glucose in a porcine experimental model of early acute respiratory distress syndrome. Design: Prospective laboratory investigation. Setting: A university animal research laboratory. Subjects: Seven piglets submitted to experimental ventilator-induced lung injury and five healthy controls. Interventions: Lung injury was induced by lung lavages and 210 minutes of injurious mechanical ventilation using low positive end-expiratory pressure and high inspiratory pressures. All animals were subsequently studied with dynamic PET imaging of [F-18]fluoro-2-deoxy-d-glucose. CT scans were acquired at end expiration and end inspiration. Measurements and Main Results: [F-18]fluoro-2-deoxy-d-glucose uptake rate was computed for the whole lung, four isogravitational regions, and regions grouping voxels with similar density. Global and intermediate gravitational zones [F-18]fluoro-2-deoxy-d-glucose uptakes were higher in ventilator-induced lung injury piglets compared with controls animals. Uptake of normally and poorly aerated regions was also higher in ventilator-induced lung injury piglets compared with control piglets, whereas regions suffering tidal recruitment or tidal hyperinflation had [F-18]fluoro-2-deoxy-d-glucose uptakes similar to controls. Conclusions: The present findings suggest that normally and poorly aerated regionscorresponding to intermediate gravitational zonesare the primary targets of the inflammatory process accompanying early experimental ventilator-induced lung injury. This may be attributed to the small volume of the aerated lung, which receives most of ventilation.
- Non-lobar atelectasis generates inflammation and structural alveolar injury in the surrounding healthy tissue during mechanical ventilation(2014) RETAMAL, Jaime; BERGAMINI, Bruno Curty; CARVALHO, Alysson R.; BOZZA, Fernando A.; BORZONE, Gisella; BORGES, Joao Batista; LARSSON, Anders; HEDENSTIERNA, Goeran; BUGEDO, Guillermo; BRUHN, AlejandroIntroduction: When alveoli collapse the traction forces exerted on their walls by adjacent expanded units may increase and concentrate. These forces may promote its re-expansion at the expense of potentially injurious stresses at the interface between the collapsed and the expanded units. We developed an experimental model to test the hypothesis that a local non-lobar atelectasis can act as a stress concentrator, contributing to inflammation and structural alveolar injury in the surrounding healthy lung tissue during mechanical ventilation. Methods: A total of 35 rats were anesthetized, paralyzed and mechanically ventilated. Atelectasis was induced by bronchial blocking: after five minutes of stabilization and pre-oxygenation with FIO2 = 1.0, a silicon cylinder blocker was wedged in the terminal bronchial tree. Afterwards, the animals were randomized between two groups: 1) Tidal volume (V-T) = 10 ml/kg and positive end-expiratory pressure (PEEP) = 3 cmH(2)O (V(T)10/PEEP3); and 2) V-T=20 ml/kg and PEEP = 0 cmH2O (V(T)20/zero end-expiratory pressure (ZEEP)). The animals were then ventilated during 180 minutes. Three series of experiments were performed: histological (n = 12); tissue cytokines (n = 12); and micro-computed tomography (microCT; n = 2). An additional six, non-ventilated, healthy animals were used as controls. Results: Atelectasis was successfully induced in the basal region of the lung of 26 out of 29 animals. The microCT of two animals revealed that the volume of the atelectasis was 0.12 and 0.21 cm(3). There were more alveolar disruption and neutrophilic infiltration in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. Edema was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in the V(T)20/ZEEP than VT10/PEEP3 group. The volume-to-surface ratio was higher in the peri-atelectasis region than the corresponding contralateral lung (control) in both groups. We did not find statistical difference in tissue interleukin-1 beta and cytokine-induced neutrophil chemoattractant-1 between regions. Conclusions: The present findings suggest that a local non-lobar atelectasis acts as a stress concentrator, generating structural alveolar injury and inflammation in the surrounding lung tissue.