Akinori Cardozo Nagato

Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs

In this study our aim was to investigate the time courses of inflammation, oxidative stress and tissue damage after hyperoxia in the mouse lung. Groups of BALB/c mice were exposed to 100% oxygen in a chamber for 12, 24 or 48 h. The controls were subjected to normoxia. The results showed that IL‐6 increased progressively after 12 (P < 0.001) and 24 h (P < 0.001) of hyperoxia with a reduction at 48 h (P < 0.01), whereas TNF‐α increased after 24 (P < 0.001) and 48 h (P < 0.001). The number of macrophages increased after 24 h (P < 0.001), whereas the number of neutrophils increased after 24 h (P < 0.01) and 48 h (P < 0.001). Superoxide dismutase activity decreased in all groups exposed to hyperoxia (P < 0.01). Catalase activity increased only at 48 h (P < 0.001). The reduced glutathione/oxidized glutathione ratio decreased after 12 h (P < 0.01) and 24 h (P < 0.05). Histological evidence of lung injury was observed at 24 and 48 h. This study shows that hyperoxia initially causes an inflammatory response at 12 h, resulting in inflammation associated with the oxidative response at 24 h and culminating in histological damage at 48 h. Knowledge of the time course of inflammation and oxidative stress prior to histological evidence of acute lung injury can improve the safety of oxygen therapy in patients.

HYPEROXIA-INDUCED LUNG INJURY IS DOSE DEPENDENT IN WISTAR RATS

Oxygen is indispensable for aerobic respiration. However, the effects of hyperoxia on the lungs are poorly defined. The aim of the present study was to determine the effects of different oxygen concentrations on rat lungs. Rats (n = 6 per group) were exposed to hyperoxia for 90 minutes at 3 different concentrations: 50% (H50%), 75% (H75%), or 100% (H100%). Bronchoalveolar lavage (BAL) was performed and the right lungs were removed for histological analyses. The BAL samples were assayed for lipid peroxidation and antioxidant status using biochemical methods. Hyperoxia induced influxes of macrophages (1.8- to 2.3-fold) and neutrophils (7.0- to 10.2-fold) into the lungs compared to the control group (exposed to normoxia; n = 6). Histological analyses of the hyperoxic groups showed hemorrhagic areas and septal edema. A significant increase (2.2-fold) in lipid peroxidation was observed in the H100% group compared to the control group (P <.05). Glutathione peroxidase and superoxide dismutase activities were reduced to approximately 20% and 40% of the control values, respectively, in all 3 hyperoxic groups, and catalase activity was reduced in both the H75% (−0.6-fold) and H100% (−0.7-fold) groups. These results indicate a harmful effect of hyperoxia on the rat lung, with evidence of oxidant/antioxidant imbalance and histological damage.

Hyperoxia promotes polarization of the immune response in ovalbumin-induced airway inflammation, leading to a TH17 cell phenotype

Previous studies have demonstrated that hyperoxia‐induced stress and oxidative damage to the lungs of mice lead to an increase in IL‐6, TNF‐α, and TGF‐β expression. Together, IL‐6 and TGF‐β have been known to direct T cell differentiation toward the TH17 phenotype. In the current study, we tested the hypothesis that hyperoxia promotes the polarization of T cells to the TH17 cell phenotype in response to ovalbumin‐induced acute airway inflammation. Airway inflammation was induced in female BALB/c mice by intraperitoneal sensitization and intranasal introduction of ovalbumin, followed by challenge methacholine. After the methacholine challenge, animals were exposed to hyperoxic conditions in an inhalation chamber for 24 h. The controls were subjected to normoxia or aluminum hydroxide dissolved in phosphate buffered saline. After 24 h of hyperoxia, the number of macrophages and lymphocytes decreased in animals with ovalbumin‐induced airway inflammation, whereas the number of neutrophils increased after ovalbumin‐induced airway inflammation. The results showed that expression of Nrf2, iNOS, T‐bet and IL‐17 increased after 24 of hyperoxia in both alveolar macrophages and in lung epithelial cells, compared with both animals that remained in room air, and animals with ovalbumin‐induced airway inflammation. Hyperoxia alone without the induction of airway inflammation lead to increased levels of TNF‐α and CCL5, whereas hyperoxia after inflammation lead to decreased CCL2 levels. Histological evidence of extravasation of inflammatory cells into the perivascular and peribronchial regions of the lungs was observed after pulmonary inflammation and hyperoxia. Hyperoxia promotes polarization of the immune response toward the TH17 phenotype, resulting in tissue damage associated with oxidative stress, and the migration of neutrophils to the lung and airways. Elucidating the effect of hyperoxia on ovalbumin‐induced acute airway inflammation is relevant to preventing or treating asthmatic patients that require oxygen supplementation to reverse the hypoxemia.

Alterations in the pulmonary histoarchitecture of neonatal mice exposed to hyperoxia

OBJECTIVES To analyze the effects of exposure to hyperoxia (100% oxygen) on the lung histoarchitecture of neonatal mice. METHODS Neonatal Balb/c mice were exposed to hyperoxia (HG) (100% oxygen) (n= 10) in a chamber (15 x 20 x 30 cm) for 24 hours with a flow of 2 L/min. The control group (CG) (n = 10) was exposed to normoxia in the same type of chamber and for the same time. After exposure, the animals were euthanized by decapitation; the lungs were removed and processed for histological examination according to the laboratory routine. Three-mm thick sections were stained with hematoxylin and eosin (H&E). The morphometric analysis was performed with in order to analyze the macrophages present in the alveolar lumen, surface density (Sv) of gas exchange, volume density (Vv) of lung parenchyma, and areas of atelectasis. RESULTS A decrease in the number of alveolar macrophages (MØ) was observed in the HG (HG = 0.08 ±0.01 MØ/mm(2), CG = 0.18 ± 0.03 MØ/mm(2), p=0.0475), Sv of gas exchange in HG (HG = 8.08 ± 0.12 mm(2)/mm(3), CG=8.65 ± 0.20mm(2)/mm(3), p = 0.0233), Vv of lung parenchyma in HG (HG = 54.7/33.5/83.5%/mm(2); CG = 75/56.7/107.9%/mm(2), p<0.0001) when compared with the CG. However, there was an increase in areas of atelectasis in HG (HG = 17.5/11.3/38.4 atelectasis/mm(2), CG = 14/6.1/24.4 atelectasis/mm(2), p=0.0166) when compared with the CG. CONCLUSION The present results indicate that hyperoxia caused alterations in lung histoarchitecture, increasing areas of atelectasis and diffuse alveolar hemorrhage.

Acromial Morphometric Analysis Using Imaging Software

El objetivo de este estudio fue medir con precision la morfologia acromial para describir los patrones anatomicos de sus subtipos y llevar a cabo un estudio de la literatura sobre las relaciones entre los subtipos morfologicos y las enfermedades relacionadas. Tomamos fotografias de la escapula del Instituto de Anatomia de la Universidad Sombra Severino, y se analizaron las imagenes con el Software Image-J®. El angulo acromial medio fue de 139,23 ± 2,781°, no habiendo diferencias significativas entre los lados derecho e izquierdo. De observo una correlacion positiva entre el angulo acromial y el angulo de la columna vertebral de la escapula. La correlacion mencionada anteriormente, juega un papel importante en los trastornos de la inflamacion del hombro, especialmente el sindrome, lo cual refuerza la importancia de los estudios de la morfologia acromial.

Protótipo de ventilação mecânica espontânea e artificial.

Current essay focuses on research with regard to pregnancy. Pregnancy brings about huge physical and psychological transformations in the female with a great variety of emotional oscillations, such as fear, anxiety, insecurity, doubts, happiness and others, which, because of the prevailing imbalance, contribute towards the start of post-partum depression symptoms. Scientific registers focusing on PPD prevention methods already demonstrate the use of psycho-social, psycho-pharmacological and hormonal strategies even though no single isolated intervention is sufficiently efficacious in the development of the disease. A review of the literature, based on on-line access to abstracts from databases, is provided. The psychotherapeutic approach is of fundamental importance in treatment, coupled to family support and follow-up.

Influência do posicionamento dos membros superiores sobre parâmetros ventilatórios em indivíduos adultos

INTRODUCTION: Pulmonary ventilation depends on the integrity of the chest wall. The positioning of the chest wall and/or the disorders of ventilatory muscles decrease the lung volume and capacity, the flow of airway pressure and inspiratory and expiratory pressures. The positioning of the upper limbs interferes with the dynamics of the chest. OBJECTIVES: To determine the effect of positioning of the arms with the shoulder 90o abduction and external rotation associated with elbow flexion to 90o on the pulmonary ventilatory function. METHODS: The subjects underwent Respiratory Questionnaire suggested by the American Thoracic Society - Division of Lung Diseases (ATS-DLD) and the individual records to search for clinical assessment of ventilatory lung function. RESULTS: We found out that the minute volume and tidal volume in healthy subjects in post-position increased when compared to the situation of pre-positioning from 9.46 ± 1.15 L/min. to 11.89 ± 1.54 L/min. and from 565.8 ± 83.84 ml to 752.4 ± 105.5 mL, respectively. CONCLUSION: The placement of members can be prioritized before lung reexpansion techniques. Pulmonary rehabilitation programs in general may include the correct positioning of the upper limbs, as this represents an advantage to muscles that act on the rib cage, improving the performance of ventilation.