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Find video protocols related to scientific articles indexed in Pubmed.
Papain-induced experimental pulmonary emphysema in male and female mice.
Respir Physiol Neurobiol
PUBLISHED: 06-02-2014
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In papain-induced models of emphysema, despite the existing extensive description of the cellular and molecular aspects therein involved, sexual hormones may play a complex and still not fully understood role. Hence, we aimed at exploring the putative gender-related differences in lung mechanics, histology and oxidative stress in papain-exposed mice. Thirty adult BALB/c mice received intratracheally either saline (50 ?L) or papain (10 U/50 ?L saline) once a week for 2 weeks. In males papain increased lung resistive and viscoelastic/inhomogeneous pressures, static elastance, and viscoelastic component of elastance, while females showed higher static elastance and resistive pressure only. Both genders presented similar higher parenchymal cellularity and mean alveolar diameter, and less collagen-elastic fiber content and body weight gain than their respective controls. Increased functional residual capacity was more prominent in males. Female papain-treated mice were more susceptible to oxidative stress. Thus, male and female papain-exposed mice respond differently, which should be carefully considered to avoid confounding results.
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Pulmonary functional and morphological damage after exposure to tripoli dust.
Respir Physiol Neurobiol
PUBLISHED: 02-13-2014
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Tripoli is a microcrystalline siliceous rock used to polish metals and precious stones. Its inhalation has been associated with increased prevalence of breathing complaints and pneumoconiosis. However, its acute human exposure has not been so far studied. We aimed at evaluating the putative mechanical, morphological, biochemical and inflammatory lung damage in mice acutely exposed to Tripoli dust. BALB/c mice were randomly assigned to 2 groups: In control group (CTRL, n=6) animals received intratracheally (i.t.) 0.9% NaCl (50?l), while Tripoli group (TRIP, n=15) received 20mg of Tripoli powder diluted in 50?L of saline i.t. The experiments were done 15 days later. TRIP mice showed higher pulmonary mechanical impedance, polymorphonuclear cells, TNF-?, IL1-? and IL-6 than CTRL. TRIP presented granulomatous nodules containing collagenous fibers that occupied 35% of the lung tissue area. In conclusion, acute exposure to Tripoli dust triggered important lung damage in mice lungs that if found in human workers could trigger severe illness.
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Time course of pulmonary burden in mice exposed to residual oil fly ash.
Front Physiol
PUBLISHED: 01-01-2014
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Residual oil fly ash (ROFA) is a common pollutant in areas where oil is burned. This particulate matter (PM) with a broad distribution of particle diameters can be inhaled by human beings and putatively damage their respiratory system. Although some studies deal with cultured cells, animals, and even epidemiological issues, so far a comprehensive analysis of respiratory outcomes as a function of the time elapsed after exposure to a low dose of ROFA is wanted. Thus, we aimed to investigate the time course of mechanical, histological, and inflammatory lung changes, as well as neutrophils in the blood, in mice exposed to ROFA until 5 days after exposure. BALB/c mice (25 ± 5 g) were randomly divided into 7 groups and intranasally instilled with either 10 ?L of sterile saline solution (0.9% NaCl, CTRL) or ROFA (0.2 ?g in 10 ?L of saline solution). Pulmonary mechanics, histology (normal and collapsed alveoli, mononuclear and polymorphonuclear cells, and ultrastructure), neutrophils (in blood and bronchoalveolar lavage fluid) were determined at 6 h in CTRL and at 6, 24, 48, 72, 96, and 120 h after ROFA exposure. ROFA contained metal elements, especially iron, polycyclic aromatic hydrocarbons (PAHs), and organochlorines. Lung resistive pressure augmented early (6 h) in the course of lung injury and other mechanical, histological and inflammatory parameters increased at 24 h, returning to control values at 120 h. Blood neutrophilia was present only at 24 and 48 h after exposure. Swelling of endothelial cells with adherent neutrophils was detected after ROFA instillation. No neutrophils were present in the lavage fluid. In conclusion, the exposure to ROFA, even in low doses, induced early changes in pulmonary mechanics, lung histology and accumulation of neutrophils in blood of mice that lasted for 4 days and disappeared spontaneously.
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Liquid- and air-filled catheters without balloon as an alternative to the air-filled balloon catheter for measurement of esophageal pressure.
PLoS ONE
PUBLISHED: 01-01-2014
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Measuring esophageal pressure (Pes) using an air-filled balloon catheter (BC) is the common approach to estimate pleural pressure and related parameters. However, Pes is not routinely measured in mechanically ventilated patients, partly due to technical and practical limitations and difficulties. This study aimed at comparing the conventional BC with two alternative methods for Pes measurement, liquid-filled and air-filled catheters without balloon (LFC and AFC), during mechanical ventilation with and without spontaneous breathing activity. Seven female juvenile pigs (32-42 kg) were anesthetized, orotracheally intubated, and a bundle of an AFC, LFC, and BC was inserted in the esophagus. Controlled and assisted mechanical ventilation were applied with positive end-expiratory pressures of 5 and 15 cmH2O, and driving pressures of 10 and 20 cmH2O, in supine and lateral decubitus.
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The influence of 5-lipoxygenase on cigarette smoke-induced emphysema in mice.
Biochim. Biophys. Acta
PUBLISHED: 06-24-2013
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Pulmonary emphysema is characterized by the loss of lung architecture. Our hypothesis is that the inhibition of 5-lipoxygenase (5-LO) production may be an important strategy to reduce inflammation, oxidative stress, and metalloproteinases in lung tissue resulting from cigarette smoke (CS)-induced emphysema.
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Redox markers and inflammation are differentially affected by atorvastatin, pravastatin or simvastatin administered before endotoxin-induced acute lung injury.
Int. Immunopharmacol.
PUBLISHED: 05-03-2013
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Statins are standard therapy for the treatment of lipid disorders, and the field of redox biology accepts that statins have antioxidant properties. Our aim in this report was to consider the pleiotropic effects of atorvastatin, pravastatin and simvastatin administered prior to endotoxin-induced acute lung injury. Male mice were divided into 5 groups and intraperitoneally injected with LPS (10 mg/kg), LPS plus atorvastatin (10 mg/kg/day; A + LPS group), LPS plus pravastatin (5 mg/kg/day; P + LPS group) or LPS plus simvastatin (20 mg/kg/day; S + LPS group). The control group received saline. All mice were sacrificed one day later. There were fewer leukocytes in the P + LPS and S + LPS groups than in the LPS group. MCP-1 cytokine levels were lower in the P + LPS group, while IL-6 levels were lower in the P + LPS and S + LPS groups. TNF-? was lower in all statin-treated groups. Levels of redox markers (superoxide dismutase and catalase) were lower in the A + LPS group (p < 0.01). The extent of lipid peroxidation (malondialdehyde and hydroperoxides) was reduced in all statin-treated groups (p < 0.05). Myeloperoxidase was lower in the P + LPS group (p < 0.01). Elastance levels were significantly greater in the LPS group compared to the statin groups. Our results suggest that atorvastatin and pravastatin but not simvastatin exhibit anti-inflammatory and antioxidant activity in endotoxin-induced acute lung injury.
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The panic disorder respiratory ratio: a dimensional approach to the respiratory subtype.
Rev Bras Psiquiatr
PUBLISHED: 04-10-2013
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The respiratory ratio is a dimensional construct of the respiratory subtype of panic disorder (PD). The respiratory subtype has been correlated with an increased sensitivity to CO? inhalation, positive family history of PD and low comorbidity with depression. The objective of our study was to determine whether the respiratory ratio is correlated with CO?-induced panic attacks and other clinical and demographic features.
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Regular exercise training attenuates pulmonary inflammatory responses to inhaled alumina refinery dust in mice.
Respir Physiol Neurobiol
PUBLISHED: 01-08-2013
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Exposure to alumina dust has been recently associated with impaired lung mechanics and inflammation. We aimed at evaluating if moderate exercise training prevents these outcomes. Twenty-three female BALB/c mice (25-30g) were randomly divided in two main groups: control (C) and exercise (E), which were submitted, or not, to 15min of swimming, 5 days/week during 4 weeks. Then, the animals were exposed for 1h to either saline solution (CS or ES) or to a suspension of 8mg/m(3) of alumina dust (CA or EA). Twenty-four hours later pulmonary mechanics was determined by the end-inflation occlusion method. Left lungs were prepared for histology and right lungs for TGF-? determination. Static elastance increased after alumina dust exposure independently of swimming. In CA group the viscoelastic component of elastance, the viscoelastic/inhomogeneous pressure, the polymorphonuclear amount, the fraction area of alveolar collapse and TGF-? increased. Thus, exercise training may mitigate the pro-inflammatory response to inhaled aluminum refinery dust.
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Endotoxin-induced acute lung injury is dependent upon oxidative response.
Inhal Toxicol
PUBLISHED: 11-30-2011
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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 ?P1 and ?P2 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 NF?B, IL-6, TNF-? 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.
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Residual oil fly ash worsens pulmonary hyperreactivity in chronic allergic mice.
Respir Physiol Neurobiol
PUBLISHED: 03-31-2011
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BALB/c mice received saline (SAL groups) or ovalbumin (OVA groups) intraperitoneally (days 1, 3, 5, 7, 9, 11 and 13). After 27 days, a burst of intratracheal OVA or SAL (days 40, 43 and 46) was performed. Animals were then divided into four groups (N=8, each) and intranasally instilled with saline (SAL-SAL and OVA-SAL) or residual oil fly ash (SAL-ROFA and OVA-ROFA). 24h later, total, initial and difference resistances (Rtot, Rinit, Rdiff) and static elastance (Est) were measured. Lung responsiveness to methacholine was assessed as slope and sensitivity of Est, Rtot, Rinit, and Rdiff. Lung morphometry (collapsed and normal areas and bronchoconstriction index) and cellularity (polymorphonuclear, mononuclear and mast cells) were determined. OVA or ROFA similarly impaired lung mechanics and increased the amount of polymorphonuclear cells and collapsed areas. OVA-ROFA showed even higher hyperresponsiveness, bronchoconstriction and mast cell infiltration. Thus, we concluded that ROFA exposure may add an extra burden to hyperresponsive lungs.
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Long-term exposure to cigarette smoke impairs lung function and increases HMGB-1 expression in mice.
Respir Physiol Neurobiol
PUBLISHED: 01-14-2011
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Cigarette smoke (CS)-induced emphysema is caused by a continuous inflammatory response in the lower respiratory tract. The development of the condition is believed to be mediated by oxidant-antioxidant imbalance. This paper describes the effects of long-term CS exposure on alveolar cell recruitment, antioxidant defense systems, activity of extracellular matrix metalloelastases, expression of metalloelastase MMP-12, and high mobility group box-1 protein (HMGB-1). Ten C57Bl/6 mice were exposed to 12 cigarettes-a-day for 60 consecutive days, while 10 control animals were exposed to ambient air. After sacrifice, bronchoalveolar lavage fluid (BALF) was removed, and lung tissue underwent biochemical and histological analyses. In CS-exposed animals influx of alveolar macrophages and neutrophils into BALF, lung static elastance, and expression of MMP-12 and HMGB-1 were significantly increased while the activity of antioxidant enzyme was significantly reduced in comparison with control group. Thus, we demonstrated for the first time that long-term CS exposure decreased antioxidant defenses concomitantly with impaired lung function, which was associated with HMGB-1 expression.
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Antispasmodic effects of eugenol on rat airway smooth muscle.
Fundam Clin Pharmacol
PUBLISHED: 11-16-2010
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This study was undertaken to assess the effects of eugenol (EUG) on tracheal muscle (TM) and the putative mechanisms underlying these effects. Cumulatively increasing concentrations (1-1000 ?m) of EUG did not affect the resting tonus of TM. However, EUG (1-2000 ?m) reduced the contractions induced by electrical field stimulation (IC(50) = 842.3 ± 52.7 ?m), an effect that was unaltered by either 10 ?m montelukast (IC(50) = 816.1?± 70.1 ?m) or 2 ?m indomethacin (IC(50) = 693.1 ± 170.8 ?m). EUG also completely relaxed the sustained contractile responses to 80 mM K(+) (IC(50) ?= 597.3 ± 60.6 ?m) and 1 ?m carbamoylcholine (IC(50) = 571.3 ± 148.8 ?m), an effect that was unaltered by indomethacin (2 ?m). Under Ca(2+) -free conditions, EUG reduced the ACh-induced contractions (IC(50) = 703.4 ± 256.1 ?m), the CaCl? -induced contractions in preparations pretreated with 60 ?m ACh in the presence of nifedipine, and the Ba(2+) -induced contractions in preparations depolarized with K(+) . In tracheal preparations maintained in Ca(2+) -containing solution, EUG (300-2000 ?m) relaxed the contractile response to phorbol dibutyrate (1 ?m), an activator of protein kinase C. It is concluded that in TM, EUG induces a myogenic antispasmodic effect (not modulated by arachidonic acid derivatives) either through various mechanisms almost with the same pharmacological potency or via an action on a step common to all of them. These mechanisms seem to include blockade of voltage- and receptor-operated Ca(2+) channels, IP? -induced Ca(2+) release from sarcoplasmic reticulum and reduction of the sensitivity of contractile proteins to Ca(2+) .
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N-(2-mercaptopropionyl)-glycine but not allopurinol prevented cigarette smoke-induced alveolar enlargement in mouse.
Respir Physiol Neurobiol
PUBLISHED: 10-26-2010
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We investigated the possible protective effects of the Allopurinol (A), N-(2-mercaptopropionyl)-glycine (M) and N-acetylcysteine (N) against lung injury caused by long-term exposure to cigarette smoke (CS) in mouse. C57BL6 mice were exposed to 12 cigarettes a day for 60 days and concomitantly treated with either one of the antioxidant drugs diluted in saline (CS+A-50 mg/kg; CS+M-200 mg/kg/day; CS+N-200 mg/kg/day). Control groups were sham-smoked (AA). Long-term CS exposure results in extensive parenchyma destruction in CS group. Both CS+N and CS+M groups showed preserved alveolar structure and showed preserved lung function when compared to CS group. Macrophage and neutrophil counts were decreased in CS+M, and CS+N groups when compared to CS group (p<0.05). Antioxidant enzyme activities were reduced in all treated groups. CS+A showed the highest reduction in catalase activity (-25%, p<0.01). We conclude that M treatment reduced long-term CS-induced inflammatory lung parenchyma destruction and lung function, comparable to N treatment, however, antioxidant administration did not reverse CS-induced antioxidant enzyme activity reduction.
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Pulmonary function and histological impairment in mice after acute exposure to aluminum dust.
Inhal Toxicol
PUBLISHED: 06-16-2010
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Along the aluminum refining process, alumina (Al2O3) constitutes the main source of dust. Although aluminum refinery workers present respiratory symptoms with lung functional changes, no conclusive data about lung function impairment after alumina exposure has been so far reported. We examined the pulmonary alterations of exposure to material collected in an aluminum refinery in Brazil. BALB/c mice were exposed in a whole-body chamber for 1 h to either saline (CTRL, n = 11) or to a suspension (in saline) of 8 mg/m(3) of the dust (ALUM, n = 11) both delivered by an ultrasonic nebulizer. Twenty-four hours after exposure lung mechanics were measured by the end-inflation method. Lungs were prepared for histology. ALUM showed significantly higher static elastance (34.61 +/- 5.76 cmH2O/mL), elastic component of viscoelasticity (8.16 +/- 1.20 cmH2O/mL), pressure used to overcome the resistive component of viscoelasticity (1.62 +/- 0.24 cmH2O), and total resistive pressure (2.21 +/- 0.49 cmH2O) than CTRL (27.95 +/- 3.63 cmH2O/mL, 6.12 +/- 0.99 cmH2O/mL, 1.23 +/- 0.19 cmH2O, and 1.68 +/- 0.23 cmH2O, respectively). ALUM also presented significantly higher fraction area of alveolar collapse (69.7 +/- 1.2%) and influx of polymorphonuclear cells (27.5 +/- 1.1%) in lung parenchyma than CTRL (27.2 +/- 1.1% and 14.6 +/- 0.7%, respectively). The composition analysis of the particulate matter showed high concentrations of aluminum. For the first time it was demonstrated in an experimental model that an acute exposure to dust collected in an aluminum producing facility impaired lung mechanics that could be associated with inflammation.
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Alternating ventilation in a rat model of increased abdominal pressure.
Respir Physiol Neurobiol
PUBLISHED: 06-15-2010
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During alternating ventilation (AV) one lung is inflating while the other is deflating. Considering the possible respiratory and hemodynamic advantages of AV, we investigated its effects during increased intra-abdominal pressure (IAP=10 mmHg). In Sprague-Dawley rats (n=6, 270-375g) the main bronchi were independently cannulated, and respiratory mechanics determined while animals underwent different ventilatory patterns: synchronic ventilation without increased IAP (SV-0), elevated IAP during SV (SV-10), and AV with elevated IAP (AV-10). Thirty-three other animals (SV-0, n=10; SV-10, n=11 and AV-10, n=12) were ventilated during 3h. Mean arterial pressure (MAP), and lung histology were assessed. Increased IAP resulted in significantly higher elastances (p<0.001), being AV-10 lower than SV-10 (p<0.020). SV-10 showed higher central venous pressure (p<0.003) than S-0; no change was observed in AV-10. Wet/dry lung weight ratio was lower in AV-10 than SV-10 (p=0.009). Application of AV reduced hemodynamic and lung impairments induced by increased IAP during SV.
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Influence of lung mechanical properties and alveolar architecture on the pathogenesis of ischemia-reperfusion injury.
Interact Cardiovasc Thorac Surg
PUBLISHED: 04-08-2010
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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.
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Roles of oxidative stress in signaling and inflammation induced by particulate matter.
Cell Biol. Toxicol.
PUBLISHED: 03-01-2010
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This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca(2+) influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.
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Paraquat (PQ)-induced pulmonary fibrosis increases exercise metabolic cost, reducing aerobic performance in rats.
J Toxicol Sci
PUBLISHED: 12-03-2009
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Rats exposed to the quaternary herbicide paraquat (PQ) exhibit oxidative stress and lung injury. In the present study, we investigated the effect of multiple exposures to PQ on aerobic performance during progressive exercise on a treadmill in rats. PQ was dissolved in saline (SAL) (10 mg/ml) and administered intraperitoneally 7 mg/kg body wt to Wistar rats (n = 5) once a week for one month. Control rats received SAL (0.7 ml/kg body wt., intraperitoneally, n = 5) over the same time period. The animals were submitted to aerobic evaluation on a treadmill using a progressive protocol until fatigue prior to the administration of the first dose of PQ or SAL and repeated at 1 week and 40 days following the last dose of the herbicide. Twenty-four hours after the last performance tests, the animals were sacrificed, lungs removed and divided in two groups: PQ and SAL for histopathological analysis. The animals exposed to PQ exhibited decrease in aerobic performance and mechanical efficiency (ME) as well as increase in oxygen consumption during exercise in comparison to the controls forty days after the last dose of PQ. Lung histologic changes included atelectasis, interstitial edema, and inflammation cells in PQ group. The collagen system fibers, fraction area of alveolar collapse and influx of polymorphonuclear (PMN) cells in lung parenchyma were higher in PQ compared to SAL. In conclusion, multiple exposures to PQ induce pulmonary fibrosis, reduce the aerobic performance and mechanical efficiency and increase the metabolic cost of exercise in rats.
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Hyperinflation using pressure support ventilation improves secretion clearance and respiratory mechanics in ventilated patients with pulmonary infection: a randomised crossover trial.
Aust J Physiother
PUBLISHED: 11-26-2009
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Is ventilator-induced hyperinflation in sidelying more effective than sidelying alone in removing secretions and improving respiratory mechanics in ventilated patients with pulmonary infection?
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[Are panic attacks really harmless? The cardiovascular impact of panic disorder].
Rev Bras Psiquiatr
PUBLISHED: 06-10-2009
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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.
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Respiratory manifestations of panic disorder: causes, consequences and therapeutic implications.
J Bras Pneumol
PUBLISHED: 01-26-2009
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Multiple respiratory abnormalities can be found in anxiety disorders, especially in panic disorder (PD). Individuals with PD experience unexpected panic attacks, characterized by anxiety and fear, resulting in a number of autonomic and respiratory symptoms. Respiratory stimulation is a common event during panic attacks. The respiratory abnormality most often reported in PD patients is increased CO2 sensitivity, which has given rise to the hypothesis of fundamental abnormalities in the physiological mechanisms that control breathing in PD. There is evidence that PD patients with dominant respiratory symptoms are more sensitive to respiratory tests than are those who do not manifest such symptoms, and that the former group constitutes a distinct subtype. Patients with PD tend to hyperventilate and to panic in response to respiratory stimulants such as CO2, triggering the activation of a hypersensitive fear network. Although respiratory physiology seems to remain normal in these subjects, recent evidence supports the idea that they present subclinical abnormalities in respiration and in other functions related to body homeostasis. The fear network, composed of the hippocampus, the medial prefrontal cortex, the amygdala and its brain stem projections, might be oversensitive in PD patients. This theory might explain why medication and cognitive-behavioral therapy are both clearly effective. Our aim was to review the relationship between respiration and PD, addressing the respiratory subtype of PD and the hyperventilation syndrome, with a focus on respiratory challenge tests, as well as on the current mechanistic concepts and the pharmacological implications of this relationship.
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Antispasmodic effects of a new kaurene diterpene isolated from Croton argyrophylloides on rat airway smooth muscle.
J. Pharm. Pharmacol.
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The effects of rel-(1S,4aS,7S,8aS)-7-(1-vinyl)-tetradecahydro-1,4a-dimethylphenanthrene-7,8a-carbolactone-1-carboxylic acid (TCCA), a new ent-kaurene diterpene isolated from Croton argyrophylloides, on rat tracheal preparations were investigated.
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Time-dependence of lung injury in mice acutely exposed to cylindrospermopsin.
Toxicon
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Cylindrospermopsin is a cyanobacterial toxin of increasing environmental importance, as it can lead to disease if orally or intravenously absorbed. However, its in vivo lung impairment has not been documented. Thus, we aimed at verifying whether cylindrospermopsin can induce lung injury and establish its putative dependence on the time elapsed since exposure. BALB/c mice were intratracheally injected with either saline (NaCl 0.9%, 50 ?L, SAL group, n = 12) or a sublethal dose (70 ?g/kg) of semi-purified extract of cylindrospermopsin (CYN groups, n = 52). Lung mechanics, histological and biochemical analyses, and cylindrospermopsin presence in lungs and liver were determined in independent groups at 2, 8, 24, 48, and 96 h after cylindrospermopsin instillation. There was a significant increase in static elastance at 24 and 48 h after exposure to cylindrospermopsin, while viscoelastic component of elastance and viscoelastic pressure rose at 48 h. Alveolar collapse augmented in CYN groups at 8 h. A significant increase in polymorphonuclear influx into lung parenchyma, as well as a higher myeloperoxidase activity started off at 24 h. Exposure to cylindrospermopsin increased lipid peroxidation and superoxide dismutase activity and reduced catalase activity in CYN groups. The toxin was detected in lungs and liver of all CYN mice. In conclusion, cylindrospermopsin exposure impaired lung mechanics, which was preceded by lung parenchyma inflammation and oxidative stress.
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High-flow nasal interface improves oxygenation in patients undergoing bronchoscopy.
Crit Care Res Pract
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During bronchoscopy hypoxemia is commonly found and oxygen supply can be delivered by interfaces fed with high gas flows. Recently, the high-flow nasal cannula (HFNC) has been introduced for oxygen therapy in adults, but they have not been used so far during bronchoscopy in adults. Forty-five patients were randomly assigned to 3 groups receiving oxygen: 40?L/min through a Venturi mask (V40, N = 15), nasal cannula (N40, N = 15), and 60?L/min through a nasal cannula (N60, N = 15) during bronchoscopy. Gas exchange and circulatory variables were sampled before (FiO(2) = 0.21), at the end of bronchoscopy (FiO(2) = 0.5), and thereafter (V40, FiO(2) = 0.35). In 8 healthy volunteers oxygen was randomly delivered according to V40, N40, and N60 settings, and airway pressure was measured. At the end of bronchoscopy, N60 presented higher PaO(2), PaO(2)/FiO(2), and SpO(2) than V40 and N40 that did not differ between them. In the volunteers (N60) median airway pressure amounted to 3.6?cmH(2)O. Under a flow rate of 40?L/min both the Venturi mask and HFNC behaved similarly, but nasal cannula associated with a 60?L/min flow produced the better results, thus indicating its use in mild respiratory dysfunctions.
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Redox imbalance and pulmonary function in bleomycin-induced fibrosis in C57BL/6, DBA/2, and BALB/c mice.
Toxicol Pathol
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The development of bleomycin-induced pulmonary fibrosis (BLEO-PF) has been associated with differences in genetic background and oxidative stress status. The authors aim was to investigate the crosstalk between the redox profile, lung histology, and respiratory function in BLEO-PF in C57BL/6, DBA/2, and BALB/c mice. BLEO-PF was induced with a single intratracheal dose of bleomycin (0.1 U/mouse). Twenty-one days after bleomycin administration, the mortality rate was over 50% in C57BL/6 and 20% in DBA/2 mice, and BLEO-PF was not observed in BALB/c. There was an increase in lung static elastance (p < .001), viscoelastic/inhomogeneous pressure (p < .05), total pressure drop after flow interruption (p < .01), and ?E (p < .05) in C57BL/6 mice. The septa volume increased in C57BL/6 (p < .05) and DBA/2 (p < .001). The levels of IFN-? were reduced in C57BL/6 mice (p < .01). OH-proline levels were increased in C57BL/6 and DBA/2 mice (p < .05). SOD activity and expression were reduced in C57BL/6 and DBA/2 mice (p < .001 and p < .001, respectively), whereas catalase was reduced in all strains 21 days following bleomycin administration compared with the saline groups (C57BL/6: p < .05; DBA/2: p < .01; BALB/c: p < .01). GPx activity and GPx1/2 expression decreased in C57BL/6 (p < .001). The authors conclude that BLEO-PF resistance may also be related to the activity and expression of SOD in BALB/c mice.
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Low tidal volume mechanical ventilation and oxidative stress in healthy mouse lungs.
J Bras Pneumol
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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.
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