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Purpose. To assess the potential effectiveness or efficacy of early mobilization on respiratory and peripheral muscle strengths and functionality in nonintubated patients. Methods. For 40 nonintubated patients over 18 years of age with over 24-hour intensive care unit (ICU) stay allocated to a single intervention, an incremental mobilization protocol was initiated. Maximal inspiratory and expiratory pressures (MIP and MEP), peripheral muscle strength (handgrip strength (HGS) and Medical Research Council scale (MRC-s)), and functionality (FIM, ICF-BMS, PFIT-s, and FSS-ICU scales) were evaluated at ICU admission and discharge. Results. All outcomes were significantly improved (pre vs. post values): MIP (43.93 ± 21.95 vs. 54.12 ± 21.68 cmH2O; P < 0.001), MEP (50.32 ± 28.65 vs. 60.30 ± 21.23; P = 0.002), HGS (25.5 (9.58) vs. 27.5 (9.48); P = 0.046), MRC-s (58.52 ± 2.84 vs. 59.47 ± 1.81; P = 0.023), FIM (54.4 ± 22.79 vs. 69.48 ± 12.74), ICF-BMS (28.63 ± 16.19 vs. 14.03 ± 11.15), PFIT-s (9.55 ± 2.34 vs. 11.18 ± 1.32) (P < 0.001), and FSS-ICU (28.7 ± 9.1 vs. 32.6 ± 5.0; P = 0.001). The ceiling effect at admission/discharge was in MRC-s (60/82.5%), FSS-ICU (50/70%), and FIM (35/62.5%). The floor effect occurred at discharge in ICF-BMS (7.5/52.5%). Conclusions. The early mobilization protocol seemed effective at maintaining/increasing the respiratory muscle strength and functionality of nonintubated patients in critical care. Ceiling effect was high for MRC-s, FSS-ICU, and FIM scales. [ABSTRACT FROM AUTHOR]

Background: Epidemiological studies have demonstrated an increased incidence of cardiovascular events in patients with bronchial asthma, but little is known about the relationship between asthma and vascular function. The purpose of this study was to evaluate endothelial function and arterial stiffness in children and adolescents with asthma.Methods: A cross-sectional controlled study was designed. Measurements of endothelial function and arterial stiffness in asthmatic (13.6 ± 0.6 years) and control groups (14.9 ± 0.7 years) were taken by the non-invasive peripheral arterial tonometry (EndoPAT2000) determined by using the natural logarithm of the reactive hyperemia index (LnRHI) and the augmentation index (AIx@75%), respectively. Patients with asthma were also administered two questionnaires to evaluate asthma control and quality of life. Exercise functional capacity was evaluated using the Shuttle Walking Test (SWT). Only male participants were included in the present study.Results: LnRHI and the walked distance during the SWT were similar between groups (p = 0.23 and p = 0.50, respectively). AIx@75% was significantly higher in the asthmatic group (-7.75 ± 1.7) compared to the control group (-15.25 ± 1.8), p < 0.04. In the control group, the LnRHI correlated positively with baseline systolic blood pressure (r = 0.53, p = 0.02) and mean arterial pressure (r = 0.50, p = 0.03), age (r = 0.61, p = 0.007), weight (r = 0.63, p = 0.004) and height (r = 0.56, p = 0.015). Besides that LnRHI correlated with FVC (r = 0.69, p = 0.002), FEV1, (r = 0.53, p = 0.03) and negatively with Tiffeneau index (FEV1/FVC%, r = -0.49 p = 0.04). The LnRHI of the asthmatic group did not correlate with the different variables evaluated.Conclusion: The increased AIx@75% without changes in LnRHI in asthmatic patients could mean that an early detection of vascular impairment may precede endothelial dysfunction, and that different mechanisms may contribute to the pathogenesis and progression of cardiovascular events in this population. A large prospective and randomized controlled study should be done to evaluate the physiopathological mechanisms underlying the association between arterial stiffness and asthma. [ABSTRACT FROM AUTHOR]

Background: The prevalence of depression in patients with chronic obstructive pulmonary disease (COPD) is associated with a worsening of prognosis. Most studies classify COPD patients as depressive or non-depressive based on symptoms, rather than on a diagnosis using specific tools. Thus, the aim of this study was to determine the impact of depression, as diagnosed by the Mini International Neuropsychiatric Interview Plus (MINI), on functional capacity estimated by the 6-minute walk test (6MWT) and unsupported upper-limb exercise test, and quality of life estimated by Saint George's Respiratory Questionnaire (SGRQ), among patients with COPD. Results: Using the MINI as a diagnostic tool, 22.2 % of all patients (6.6 % of all men and 41.6 % of all women) were diagnosed with depression. No significant differences were found between depressive and non-depressive patients with regard to anthropometric measurements, lung function, functional capacity, or quality of life variables. The best models for the dependent variables representing functional capacity and quality of life revealed that the covariates SGRQTOTAL and gender (R2 = 16.7 %) were significant in explaining the response variable for functional capacity of the upper limbs. Results also showed that age, monthly income, insomnia, and the results of a 6MWT were significant in explaining overall quality of life (R²2 = 46 %), and that the percentage of the predicted forced expiratory volume in the first second post-bronchodilator and gender were significant in explaining walking distance (R² = 22 %). Depression, as diagnosed by the MINI, was not significant in explaining any of the dependent variables. Conclusions: Despite a high prevalence of depression in COPD patients, especially in women, depression, as diagnosed by the MINI, was not correlated with functional capacity tests or quality of life in patients with moderate to very severe COPD in the present study. This suggests that depression identified by this diagnostic test may be more accurate than depression diagnosed by tests that evaluate symptoms, as they may be influenced by the perceptions of the patient in relation to their health. [ABSTRACT FROM AUTHOR]

The angiotensin-(1-7) [ANG-(1-7)]/Mas receptor pathway is currently recognized as a counterbalancing mechanism of the renin-angiotensin system in different pathophysiological conditions. We have previously described that treatment with ANG-(1-7) attenuates lung inflammation and remodeling in an experimental model of asthma. In the present study, we investigated whether lack of the Mas receptor could alter the inflammatory response in a model of chronic allergic lung inflammation induced by ovalbumin (OVA). Mas receptor wild-type (MasWT) and knockout (MasKO) mice were subjected to four doses of OVA (20 μg/mice ip) with a 14-day interval. At the 21st day, nebulization with OVA (1%) was started, three times per week until the 46th day. Control groups received saline (0.9% ip) and were nebulized with saline (0.9%). MasWT-OVA developed a modest inflammatory response and minor pulmonary remodeling to OVA challenge. Strikingly, MasKO-OVA presented a significant increase in inflammatory cell infiltrate, increase in extracellular matrix deposition, increase in thickening of the alveolar parenchyma, increase in thickening of the smooth muscle layer of the pulmonary arterioles, increase in proinflammatory cytokine and chemokine levels in the lungs, characteristic of chronic asthma. Additionally, MasKO-OVA presented an increase in ERK1/2 phosphorylation compared with MasWT-OVA. Furthermore, MasKO-OVA showed a worse performance in a test of maximum physical exercise compared with MasWT-OVA. Our study shows that effects triggered by the Mas receptor are important to attenuate the inflammatory and remodeling processes in a model of allergic lung inflammation in mice. Our data indicate that impairment of the ANG-(1-7)/Mas receptor pathway may lead to worsening of the pathophysiological changes of asthma., (Copyright © 2016 the American Physiological Society.)

Purpose: Patients with pulmonary fibrosis often exhibit reduced lung function and diminished health-related quality of life. Studies have shown that paraquat-induced, extrapulmonary, acute lung injury affects the metabolic profile of glycogen content in different tissues. The purpose of the present study was to investigate whether the process of pulmonary fibrosis induced by continuous exposure to the toxic herbicide paraquat or by a local insult from bleomycin affects the glycogen content in tissues., Methods: In the paraquat experiment, Wistar rats (n = 5 per group) received either saline (controls) or an intraperitoneal injection of a paraquat solution (7.0 mg/kg; experimental group) once a week for 4 weeks. In the bleomycin experiment, Balb/c mice (n = 5 per group) received either saline (controls) or 6.25 U/kg of bleomycin through intratracheal instillation in single dose (experimental group). Glycogen content in different tissues (mg/g tissue) was measured using the anthrone reagent. The lungs submitted to histopathological and quantitative analyses of fibrosis., Results: Paraquat-induced fibrosis led to lower glycogen content in the gastrocnemius muscle (2.7 ± 0.1 vs. 3.4 ± 0.1; 79 %) compared with the controls, whereas no changes in glycogen content were found in the diaphragm or heart. Bleomycin-induced fibrosis led to lower glycogen content in the diaphragm (0.43 ± 0.02 vs. 0.79 ± 0.09, 54 %), gastrocnemius muscle (0.62 ± 0.11 vs. 1.18 ± 0.06, 52 %), and heart (0.68 ± 0.11 vs. 1.39 ± 0.1, 49 %) compared with the controls (p < 0.05). Moreover, the area of fibrous connective tissue (μm(2)) in the lungs was significantly increased in paraquat-induced fibrosis (3,463 ± 377 vs. 565 ± 89) and bleomycin-induced fibrosis (3,707 ± 433.9 vs. 179 ± 51.28) compared with the controls., Conclusions: The findings suggest that the effects of fibrogenesis in the lungs are not limited to local alterations but also lead to a reduction in glycogen content in the heart and other muscles. This reduction could partially explain the impaired muscle performance found in patients with pulmonary fibrosis.