JOAO BATISTA BORGES SOBRINHO DORINI
Projetos de Pesquisa
Unidades Organizacionais
LIM/09 - Laboratório de Pneumologia, Hospital das Clínicas, Faculdade de Medicina
2 resultados
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- There is no cephalocaudal gradient of computed tomography densities or lung behavior in supine patients with acute respiratory distress syndrome(2016) EL-DASH, S. A.; BORGES, J. B.; COSTA, E. L. V.; TUCCI, M. R.; RANZANI, O. T.; CARAMEZ, M. P.; CARVALHO, C. R. R.; AMATO, M. B. P.Background: There is debate whether pressure transmission within the lungs and alveolar collapse follow a hydrostatic pattern or the compression exerted by the weight of the heart and the diaphragm causes collapse localized in the areas adjacent to these structures. The second hypothesis proposes the existence of a cephalocaudal gradient in alveolar collapse. We aimed to define whether or not lung density and collapse follow a 'liquid-like' pattern with homogeneous isogravitational layers along the cephalocaudal axis in acute respiratory distress syndrome lungs. Methods: Acute respiratory distress syndrome patients were submitted to full lung computed tomography scans at positive end-expiratory pressure (PEEP) zero (before) and 25 cmH(2)O after a maximum-recruitment maneuver. PEEP was then decreased by 2 cmH2O every 4 min, and a semi-complete scan performed at the end of each PEEP step. Results: Lung densities were homogeneous within each lung layer. Lung density increased along the ventrodorsal axis toward the dorsal region (beta = 0.49, P < 0.001), while there was no increase, but rather a slight decrease, toward the diaphragm along the cephalocaudal axis and toward the heart. Higher PEEP attenuated density gradients. At PEEP 18 cmH2O, dependent lung regions started to collapse massively, while best compliance was only reached at a lower PEEP. Conclusions: We could not detect cephalocaudal gradients in lung densities or in alveolar collapse. Likely, external pressures applied on the lung by the chest wall, organs, and effusions are transmitted throughout the lung in a hydrostatic pattern with homogeneous consequences at each isogravitational layer. A single cross-sectional image of the lung could fully represent the heterogeneous mechanical properties of dependent and non-dependent lung regions.
- Cell Therapy for Fibrotic Interstitial Pulmonary Disease: Experimental Study(2011) CABRAL, Rosa M.; BRANCO, Erika; RIZZO, Marcia Dos S.; FERREIRA, Guilherme J.; GREGORES, Guilherme B.; SAMOTO, Vivian Y.; STOPIGLIA, Angelo J.; MAIORKA, Paulo C.; FIORETTO, Emerson T.; CAPELOZZI, Vera L.; BORGES, Joao B.; GOMES, Susimeire; BERALDO, Marcelo A.; CARVALHO, Carlos R. R.; MIGLINO, Maria A.Parte superior do formulario Digite um texto ou endereco de um site ou traduza um documento. The aim of this study is to evaluate the histological changes in lung parenchyma of pigs affected by interstitial lung disease induced after the infusion of bone marrow mononuclear cells (BMMCs). Ten female swines were submitted to pulmonary fibrosis induced by a single dose of intratracheal bleomicine sulfate. Animals were arranged into two groups: Group 1: induced-disease control and Group 2: cell therapy using BMMCs. Both groups were clinically evaluated for 180 days. High-resolution computed tomography (HRCT) was performed at 90 and 180 days. BMMC sampling was performed in cell therapy group at 90 days. Euthanasia was performed, and samples were collected for histology and immunohistochemistry. The 90-days HRCT demonstrated typical interstitial lesions in pulmonary parenchyma similarly to human disease. The 180-days HRCT in Group 1 demonstrated advanced stages of the disease when compared with Group 2. Immunohistochemistry analysis suggests the presence of pre-existent vessels and neoformed vessels as well as predominant young cells in the injured parenchyma of Group 2. Immunohistochemistry analysis suggests that cell therapy would promote a reconstructive response. Histology and HRCT analysis suggest a positive application of swine as a model for a bleomicine inducing of fibrotic interstitial pulmonary disease. Microsc. Res. Tech. 74:957-962, 2011. (C) 2011 Wiley-Liss, Inc.