Thaís Fernanda Fazza
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Thaís Fernanda Fazza has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Bruno Curty Bergamini
Divisão de Cuidados Pulmonares Intensivos, Universidade Federal de Juiz de Fora, Juiz de Fora, Brazil, Brazil
1 shared publication - Bruno Valle Pinheiro
Pulmonary and Critical Care Division, Hospital Universitário, Universidade Federal de Juiz de Fora - Juiz de Fora (MG), Brazil
1 shared publication - Erich Vidal Carvalho
Department of Respiratory Medicine, Medical School, Federal University of Juiz de Fora, Juiz de Fora, Brazil
1 shared publication - Gabriele Moura Lopes
Pulmonary and Critical Care Division, Hospital Universitário, Universidade Federal de Juiz de Fora - Juiz de Fora (MG), Brazil
1 shared publication - Juliana Dias Nascimento Ferreira
Divisão de Pneumologia e Terapia Intensiva, Hospital Universitário, Universidade Federal de Juiz de Fora, Juiz de Fora (MG), Brasil
1 shared publication - Leda Marília Fonseca Lucinda
Universidade Federal de Juiz de Fora, Brazil; Universidade Federal de Juiz de Fora, Brazil
1 shared publication
Latest Publications
- Open Access
- 1 January 2023
- Published by Associação de Medicina Intensiva Brasileira in Critical Care Science
- Vol. 35 (4) , 386-393
Effects of atelectatic areas on the surrounding lung tissue during mechanical ventilation in an experimental model of acute lung injury induced by lipopolysaccharide
To assess the effect of atelectasis during mechanical ventilation on the periatelectatic and normal lung regions in a model of atelectasis in rats with acute lung injury induced by lipopolysaccharide. Twenty-four rats were randomized into the following four groups, each with 6 animals: the Saline-Control Group, Lipopolysaccharide Control Group, Saline-Atelectasis Group, and Lipopolysaccharide Atelectasis Group. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide. After 24 hours, atelectasis was induced by bronchial blocking. The animals underwent mechanical ventilation for two hours with protective parameters, and respiratory mechanics were monitored during this period. Thereafter, histologic analyses of two regions of interest, periatelectatic areas and the normally-aerated lung contralateral to the atelectatic areas, were performed. The lung injury score was significantly higher in the Lipopolysaccharide Control Group (0.41 ± 0.13) than in the Saline Control Group (0.15 ± 0.51), p < 0.05. Periatelectatic regions showed higher lung injury scores than normally-aerated regions in both the Saline-Atelectasis (0.44 ± 0.06 x 0.27 ± 0.74 p < 0.05) and Lipopolysaccharide Atelectasis (0.56 ± 0.09 x 0.35 ± 0.04 p < 0.05) Groups. The lung injury score in the periatelectatic regions was higher in the Lipopolysaccharide Atelectasis Group (0.56 ± 0.09) than in the periatelectatic region of the Saline-Atelectasis Group (0.44 ± 0.06), p < 0.05. Atelectasis may cause injury to the surrounding tissue after a period of mechanical ventilation with protective parameters. Its effect was more significant in previously injured lungs.
- 1 January 2023
- Published by Associação de Medicina Intensiva Brasileira in Critical Care Science
- Vol. 35 (4) , 386-393
Open AccessEffects of atelectatic areas on the surrounding lung tissue during mechanical ventilation in an experimental model of acute lung injury induced by lipopolysaccharide
To assess the effect of atelectasis during mechanical ventilation on the periatelectatic and normal lung regions in a model of atelectasis in rats with acute lung injury induced by lipopolysaccharide. Twenty-four rats were randomized into the following four groups, each with 6 animals: the Saline-Control Group, Lipopolysaccharide Control Group, Saline-Atelectasis Group, and Lipopolysaccharide Atelectasis Group. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide. After 24 hours, atelectasis was induced by bronchial blocking. The animals underwent mechanical ventilation for two hours with protective parameters, and respiratory mechanics were monitored during this period. Thereafter, histologic analyses of two regions of interest, periatelectatic areas and the normally-aerated lung contralateral to the atelectatic areas, were performed. The lung injury score was significantly higher in the Lipopolysaccharide Control Group (0.41 ± 0.13) than in the Saline Control Group (0.15 ± 0.51), p < 0.05. Periatelectatic regions showed higher lung injury scores than normally-aerated regions in both the Saline-Atelectasis (0.44 ± 0.06 x 0.27 ± 0.74 p < 0.05) and Lipopolysaccharide Atelectasis (0.56 ± 0.09 x 0.35 ± 0.04 p < 0.05) Groups. The lung injury score in the periatelectatic regions was higher in the Lipopolysaccharide Atelectasis Group (0.56 ± 0.09) than in the periatelectatic region of the Saline-Atelectasis Group (0.44 ± 0.06), p < 0.05. Atelectasis may cause injury to the surrounding tissue after a period of mechanical ventilation with protective parameters. Its effect was more significant in previously injured lungs.