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Objective: To evaluate the different components of the resistance of the respiratory system, respiratory muscle strength and to investigate the occurrence of expiratory flow limitation (EFL) in patients with morbid obesity (MO) when seated. Methods: The sample was composed of MO (BMI≥40 kg/m2) and non-obese individuals (NO) with a BMI between 18 and 30 kg/m2. The protocol consisted of the anthropometric assessment and the following measures of respiratory function: spirometry, maximal inspiratory and expiratory pressures (MIP and MEP, respectively) and impulse oscillometry. The group comparison was performed using T-test for unpaired samples. The correlations were evaluated by the Pearson test with a significance level of 5%. Results: F ifty M O (age 40±10.4 years, 1.64±0.09 m, 138.8±33.6 kg and 50.7±8.9 kg/m2), and 30 NO (age 37.6±11.5 years, 1.67±0.09 m, 65.2±10.3 kg and 23.2±22 kg/m2) were evaluated. The MO showed higher values of total, peripheral, airways, tissue and central resistance when compared to the NO. No patient showed EFL. The waist circumference was associated with spirometric variables, MIP, and MEP. The waist-to-hip ratio was correlated to respiratory mechanics and spirometric variables, MIP, and MEP. Conclusion: Morbidly obese patients with no obstructive spirometric pattern show increased total, airway, peripheral, and tissue respiratory system resistance when compared to nonobese. These individuals, however, do not present with expiratory flow limitation and reduced respiratory muscles strength. [ABSTRACT FROM AUTHOR]

Copyright of Brazilian Journal of Pulmonology / Jornal Brasileiro de Pneumologia is the property of Sociedade Brasileira de Pneumologia e Tisiologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of the present study was to investigate the involvement of oxidative stress in acute lung injury (ALI) induced by lipopolysaccharide (LPS) and its effects upon cell structure, function and inflammation. In total, 108 male C57BL/6 mice were divided into seven groups: CTR Group (50 µL of saline) administered intratracheally (i.t.), LPS 6 h (10 µg of LPS − i.t.), LPS 12 h (10 µg of LPS − i.t.), LPS 24 h (10 µg of LPS − i.t.), LPS 48 h (10 µg of LPS − i.t.), LPS 24 h (10 µg − i.t.) ++ NAC 40 mg/kg (gavage) and 24 h LPS (10 µg − i.t.) ++ NAC 100 mg/kg (gavage). The antioxidant treatment protected the lungs from stress in the first 12 h, but significant oxidative stress induction was observed at the 24-hour time point, and, after 48 h, there was no protection exerted by the antioxidant treatment. NAC (N-acetylcysteine) reversed the elastance parameters, and ΔP1 and ΔP2 compared with 24 h LPS alone. NAC reduced the number of inflammatory cells in histology analysis when compared with the 24 h LPS alone-treated group. NAC also inhibited the transcription of NFκB, IL-6, TNF-α and COX2 usually induced by LPS. Our results suggest that oxidative stress plays an important role in structural, functional and inflammatory responses in the ALI model. [ABSTRACT FROM AUTHOR]

Copyright of Brazilian Journal of Pulmonology / Jornal Brasileiro de Pneumologia is the property of Sociedade Brasileira de Pneumologia e Tisiologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Psychosocial stress and depression have already been established as risk factors for developing and worsening cardiovascular diseases. Anxiety disorders are been strongly associated to cardiac problems nowadays. Panic disorder in cardiac patients represents a challenge for diagnose and treatment. Update the reader on the status of the association between anxiety disorders, particularly panic disorder, in cardiac patients. Method: Were retrieved papers published at ISI and Medline databases since 1998. Key-words used were: "heart disease", "coronary disease", "anxiety", "panic disorder" and "autonomic function". Discussion: The characteristic autonomic pattern found in patients with panic disorder, particularly the reduction in heart rate variability, are discussed as potential mediators of the cardiovascular impact of panic disorder. Conclusions: Despite de established association between panic disorder and cardiac diseases, current literatures data points to a knowledge gap on treating and diagnosing the comorbidity between panic disorder and cardiovascular diseases. Cognitive-behavioral therapy and regular supervised exercise are recommended as potential adjunct therapeutic interventions. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the different components of the resistance of the respiratory system, respiratory muscle strength and to investigate the occurrence of expiratory flow limitation (EFL) in patients with morbid obesity (MO) when seated., Methods: The sample was composed of MO (BMI≥40 kg/m2) and non-obese individuals (NO) with a BMI between 18 and 30 kg/m2. The protocol consisted of the anthropometric assessment and the following measures of respiratory function: spirometry, maximal inspiratory and expiratory pressures (MIP and MEP, respectively) and impulse oscillometry. The group comparison was performed using T-test for unpaired samples. The correlations were evaluated by the Pearson test with a significance level of 5%., Results: Fifty MO (age 40±10.4 years, 1.64±0.09 m, 138.8±33.6 kg and 50.7±8.9 kg/m2), and 30 NO (age 37.6±11.5 years, 1.67±0.09 m, 65.2±10.3 kg and 23.2±22 kg/m2) were evaluated. The MO showed higher values of total, peripheral, airways, tissue and central resistance when compared to the NO. No patient showed EFL. The waist circumference was associated with spirometric variables, MIP, and MEP. The waist-to-hip ratio was correlated to respiratory mechanics and spirometric variables, MIP, and MEP., Conclusion: Morbidly obese patients with no obstructive spirometric pattern show increased total, airway, peripheral, and tissue respiratory system resistance when compared to nonobese. These individuals, however, do not present with expiratory flow limitation and reduced respiratory muscles strength.

Ovalbumin-induced allergic lung inflammation (ALI) is a condition believed to be mediated by cytokines, extracellular matrix remodeling, and redox imbalance. In this study, we evaluated pulmonary function together with inflammatory markers as interleukin-4 (IL-4), myeloperoxidase (MPO), eosinophil cells, and redox markers in the lungs of BALB/c mice after ovalbumin (OVA) sensitization and challenge. Our results showed an increase in bronchial hyperresponsiveness stimulated by methacholine (Mch), inflammatory cell influx, especially eosinophils together with an increase of high mobility group box 1 (HMGB1) and altered lipid peroxidation (LP) and antioxidant defenses in the OVA group compared to the control group (p ≤ 0.5). Thus, we demonstrated that OVA-induced ALI altered redox status concomitantly with impaired lung function, which was associated with HMGB1 expression and proteolytic remodeling. Taken together all results found here, we may suggest HMGB1 is an important therapeutic target for asthma, once orchestrates the redox signaling, inflammation, and remodeling that contribute to the disease development.

Objective: Mechanical ventilation (MV) itself can directly contribute to lung injury. Therefore, the aim of the present study was to investigate early biomarkers concerning oxidant/antioxidant balance, oxidative stress, and inflammation caused by short-term MV in healthy mouse lungs., Methods: Twenty male C57BL/6 mice were randomly divided into two groups: MV, submitted to low tidal volume (V T, 6 mL/kg) MV for 30 min; and spontaneous respiration (SR), used as controls. Lung homogenate samples were tested regarding the activity of various antioxidant enzymes, lipid peroxidation, and TNF-α expression., Results: In comparison with the SR group, the MV group showed a significant decrease in the activity of superoxide dismutase (≈35%; p < 0.05), together with an increase in the activity of catalase (40%; p < 0.01), glutathione peroxidase (500%; p < 0.001), and myeloperoxidase (260%; p < 0.001), as well as a reduction in the glutathione/oxidized glutathione ratio (≈50%; p < 0.05) and an increase in TNF-α expression in the MV group. Oxidative damage, assessed by lipid peroxidation, was also greater in the MV group (45%; p < 0.05)., Conclusions: Our results show that short-term low V T MV can directly contribute to lung injury, generating oxidative stress and inflammation in healthy mouse lungs.

We tested the hypothesis that lung preservation techniques disarrange lung architecture, increase pulmonary impedance and lead to ischemia-reperfusion injury, which can be prevented by re-establishment of optimal lung geometry. In the first phase, fresh, cold ischemic, preserved lungs insufflated to total lung capacity (TLC) and preserved lungs ventilated with tidal volume prior to reperfusion were submitted to a 60-min ex-vivo reperfusion to evaluate the gas exchange, pulmonary hemodynamic and lung mechanics' properties. In the second phase, we evaluated the mechanical properties of lungs submitted to the same conditions of the first phase. Cold ischemic lungs developed fulminant edema during the first 15 min of ex-vivo reperfusion, whereas gas exchange, hemodynamic and mechanic properties of lungs insufflated to TLC and ventilated during 10 min prior to reperfusion were similar to fresh lungs. After the pulmonary vascular flush pulmonary impedance and alveolar collapsed area increased significantly. The insufflation to TLC and 10 min of tidal ventilation reduced the lung impedance and the percentage of alveolar collapsed area. Lung preservation techniques disarrange alveolar architecture, which lead to ischemia-reperfusion injury; recruitment maneuvers decrease the pulmonary inhomogeneities and protect the lungs against the ischemia-reperfusion injury.

Background and Objectives: An inspired oxygen fraction (FiO2) of 40% is often used for weaning patients, but lower FiO2 values are also recommended, if arterial oxygen pressure (PaO2)/ FiO2 >150-200 mmHg. This study aimed to compare respiratory variables and vital data values recorded during use of sufficient FiO2 (ideal) to maintain peripheral oxygen saturation at 92% with values recorded during use of FiO2 established at 40% (baseline) in weaning patients., Methods: Prospective cross-over study. Respiratory variables (respiratory frequency, tidal volume, occlusion pressure, inspiratory time/total time ratio) and vital data (blood pressure and heart rate) were collected sequentially at 30 and 60 minutes with baseline FiO2, followed by ideal FiO2. These were compared to a generalized linear model for repeated measurements. Comparisons between baseline and ideal FiO2 values, and arterial blood gases were evaluated by the Student's t or Wilcoxon tests., Results: In 30 adult patients the median of ideal FiO2 was 25% (IQ25%-75% 23-28). This was significantly lower than baseline FiO2 (40%) (p< 0.001). No significant difference was found in the PaO2/ FiO2 ratio between baseline FiO2 (269±53) and ideal FiO2 (268±47). Tidal volume was significantly lower during use of ideal FiO2 (p=0.003) and blood pressure was significantly higher during use of baseline FiO2 (p=0.041), but there was no clinical significance. The remaining variables were not affected by reduction in FiO2. The ideal FiO2 did not influence remaining variables., Conclusions: These results suggest that FiO2 levels sufficient to ensure a SpO2>92% did not alter breathing patterns or trigger clinical changes in weaning patients.