Maior A.S.,Carlos Chagas Filho Biophysics Institute |
Maior A.S.,Plinio Leite University |
Menezes P.,Post Graduate Physical Education Program |
Pedrosa R.C.,Clementino Fraga Filho University Hospital |
And 3 more authors.
Clinical and Experimental Pharmacology and Physiology | Year: 2010
1. The aim of the present study was to investigate the cardiovascular effects of anabolic androgenic steroid (AAS) abuse by comparing the electrocardiographic parameters before and after submaximal exercise between AAS users and non-AAS users. 2. A total of 22 men who regularly engaged in both resistance and aerobic exercise at fitness academies volunteered for the study (control group: n = 11, age 25 ± 4 years; AAS group: n = 11, age 27 ± 5 years). All subjects were submitted to submaximal exercise testing using an Astrand-Rhyming protocol. Heart rate and electrocardiography parameters were measured at rest and at the third minute of the post-exercise recovery time. 3. AAS users presented higher QTc and QTd at rest (10% and 55%, respectively) and at the post-exercise period (17% and 43%, respectively), compared with control subjects. The maximal and minimum QTc interval of the AAS group was significantly prolonged at the post-exercise period (12% and 15%, respectively). The haemodynamic parameters were similar in both groups (P > 0.05). The AAS group showed a lower heart rate recovery at the first minute after the test (P = 0.0001), and a higher exertion score (P < 0.0001) at a lower workload, compared with the control group. 4. Our results show that the QTc interval and dispersion are increased in individuals who abuse AAS, suggesting the presence of ventricular repolarization abnormalities that could potentially increase the risk of cardiac arrhythmias and sudden cardiac death. © 2010 The Authors. Clinical and Experimental Pharmacology and Physiology © 2010 Blackwell Publishing Asia Pty Ltd.
Oliveira G.P.,Federal University of Rio de Janeiro |
Silva J.D.,Federal University of Rio de Janeiro |
De Araujo C.C.,Federal University of Rio de Janeiro |
Prota L.F.M.,Carlos Chagas Filho Biophysics Institute |
And 9 more authors.
Shock | Year: 2014
Malnutrition is a risk factor for infection, compromising immune response. Glutamine (Gln) protects the lungs and distal organs in well-nourished septic and nonseptic conditions; however, no study to date has analyzed the effects of Gln in the presence of sepsis and malnutrition. In the present work, we tested the hypothesis that early therapy with intravenous Gln prevents lung and distal organ damage in septic malnourished rats. Protein-energy malnutrition was induced in male Wistar rats for 4 weeks. At the end of 4 weeks, malnourished animals were assigned to a sepsis-inducing cecal ligation and puncture group or a sham surgery group. One hour after surgery, animals were given saline (Sal) or L-alanyl-L-glutamine (Gln) intravenously. In addition, a control group (C) was set up with rats fed ad libitum, not submitted to surgery or treatment. Forty-eight hours after surgery, in malnutrition-sham rats, Gln therapy lessened neutrophil lung infiltration and apoptosis in lung and liver. In malnutrition-cecal ligation and puncture rats, Gln therapy yielded (a) reduced static lung elastance, alveolar collapse, inflammation (neutrophil infiltration, interleukin 6), and collagen deposition; (b) repair of types I and II epithelial cells; (c) no significant changes in heat shock protein 70 expression or heat shock factor 1 phosphorylation; (d) a greater number of M1 and M2 macrophages in lung tissue; and (e) less apoptosis in the lung, kidney, small intestine, and liver. In conclusion, early therapy with intravenous Gln reduced inflammation, fibrosis, and apoptosis, minimizing lung and distal organ injury, in septic malnourished rats. These beneficial effects may be associated with macrophage activation in the lung. © 2014 by the Shock Society.
Paredes B.D.,Carlos Chagas Filho Biophysics Institute |
Faccioli L.A.P.,Carlos Chagas Filho Biophysics Institute |
Quintanilha L.F.,Carlos Chagas Filho Biophysics Institute |
Asensi K.D.,Carlos Chagas Filho Biophysics Institute |
And 5 more authors.
World Journal of Hepatology | Year: 2012
Aim: To investigate the contribution of bone marrow (BM) cells to hepatic fibrosis. Methods: To establish a model of chimerism, C57Bl/6 female mice were subjected to full-body irradiation (7 Gy) resulting in BM myeloablation. BM mononuclear cells obtained from male transgenic mice expressing enhanced green fluorescent protein (GFP) were used for reconstitution. Engraftment was confirmed by flow cytometry. To induce liver injury, chimeric animals received carbon tetrachloride (CCl4) 0.5 mL/kg intraperitoneally twice a week for 30 d (CCl4 30 d) and age-matched controls received saline (Saline 30 d). At the end of this period, animals were sacrificed for post mortem analysis. Liver samples were stained with hematoxylin and eosin to observe liver architectural changes and with Sirius red for collagen quantification by morphometric analysis. α-smooth muscle actin (α-SMA) was analyzed by confocal microscopy to identify GFP+ cells with myofibroblast (MF) characteristics. Liver tissue, BM and peripheral blood were collected and prepared for flow cytometric analysis using specific markers for detection of hepatic stellate cells (HSCs) and precursors from the BM. Results: Injury to the liver induced changes in the hepatic parenchymal architecture, as reflected by the presence of inflammatory infiltrate and an increase in collagen deposition (Saline 30 d = 11.10% ± 1.12% vs CCl4 30 d = 12.60% ± 0.73%, P = 0.0329). Confocal microscopy revealed increased reactivity against a-SMA in CCl4 30 d compared to Saline 30 d, but there was no co-localization with GFP+ cells, suggesting that cells from BM do not differentiate to MFs. Liver flow cytometric analysis showed a significant increase of CD45+/ GFP+ cells in liver tissue (Saline 30 d = 3.2% ± 2.2% vs CCl4 30 d = 5.8% ± 1.3%, P = 0.0458), suggesting that this increase was due to inflammatory cell infiltration (neutrophils and monocytes). There was also a significant increase of common myeloid progenitor cells (CD117+/CD45+) in the livers of CCl4-treated animals (Saline 30 d = 2.16% ± 1.80% vs CCl4 30 d = 5.60% ± 1.30%, P = 0.0142). In addition the GFP-/CD38+/ CD45- subpopulation was significantly increased in the CCl4 30 d group compared to the Saline 30 d group (17.5% ± 3.9% vs 9.3% ± 2.4%, P = 0.004), indicating that the increase in the activated HSC subpopulation was not of BM origin. Conclusion: BM progenitor cells do not contribute to fibrosis, but there is a high recruitment of inflammatory cells that stimulates HSCs and MFs of liver origin. © 2012 Baishideng.
Magalhaes C.B.,Carlos Chagas Filho Biophysics Institute |
Riva D.R.,Carlos Chagas Filho Biophysics Institute |
Depaula L.J.,Carlos Chagas Filho Biophysics Institute |
Brando-Lima A.,Federal University of Rio de Janeiro |
And 4 more authors.
Journal of Applied Physiology | Year: 2010
Eugenol, a methoxyphenol component ot clove oil, suppresses cyciooxygenase-2 expression, while eugenol dimers prevent nuclear factor-κβ (NF-κβ) activation and inflammatory cytokine expression in lipopolysaccharide-stimulated macrophages. Our aim was to examine the in vivo anti-inflammatory effects of eugenol. BALB/c mice were divided into four groups. Mice received saline [0.05 ml intratracheally (it), control (Ctrl) and eugenol (Eug) groups] or Escherichia coli LPS (10 μg it, LPS and LPSEug groups). After 6 h, mice received saline (0.2 ml ip, Ctrl and LPS groups) or eugenol (160 mg/kg ip, Eug and LPSEug groups). Twenty-four hours after LPS injection pulmonary resistive (ΔP1) and viscoelastic (ΔP2) pressures, static elastance (Est), and viscoelastic component of elastance (ΔΕ) were measured. Lungs were prepared for histology. In parallel mice, bronchoalveolar lavage fluid was collected 24 h after LPS injection. TNF-α was determined by ELISA. Lung tissue expression of NF-κΒ was determined by EMSA. ΔP1, ΔP2, Est and ΔΕ were significantly higher in the LPS group than in the other groups. LPS mice also showed significantly more alveolar collapse, collagen fibers, and neutrophil influx and higher TNF-α levels and NF-κΒ expression than the other groups. Eugenol treatment reduced LPS-induced lung inflammation, improving lung function. Our results suggest that eugenol exhibits in vivo anti-inflammatory action in LPS-induced lung injury. Copyright © 2010 the American Physiological Society.
Antunes M.A.,Carlos Chagas Filho Biophysics Institute |
Abreu S.C.,Carlos Chagas Filho Biophysics Institute |
Silva A.L.,Carlos Chagas Filho Biophysics Institute |
Parra-Cuentas E.R.,University of Sao Paulo |
And 6 more authors.
Journal of Applied Physiology | Year: 2010
There is evidence that sex and sex hormones influence the severity of asthma. Airway and lung parenchyma remodeling and the relationship of ultrastructural changes to airway responsiveness and inflammation in male, female, and oophorectomized mice (OVX) were analyzed in experimental chronic allergic asthma. Seventy-two BALB/c mice were randomly divided into three groups (n = 24/each): male, female, and OVX mice, whose ovaries were removed 7 days before the start of sensitization. Each group was further randomized to be sensitized and challenged with ovalbumin (OVA) or saline. Twenty-four hours after the last challenge, collagen fiber content in airways and lung parenchyma, the volume proportion of smooth muscle-specific actin in alveolar ducts and terminal bronchiole, the amount of matrix metalloproteinase (MMP)-2 and MMP-9, and the number of eosinophils and interleukin (IL)-4, IL-5, and transforming growth factor (TGF)-β levels in bronchoalveolar lavage fluid were higher in female than male OVA mice. The response of OVX mice was similar to that of males, except that IL-5 remained higher. Nevertheless, after OVA provocation, airway responsiveness to methacholine was higher in males compared with females and OVX mice. In conclusion, sex influenced the remodeling process, but the mechanisms responsible for airway hyperresponsiveness seemed to differ from those related to remodeling. Copyright © 2010 the American Physiological Society.