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1.
Physiol Meas ; 35(2): 177-88, 2014 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-24398394

RESUMEN

Tracheal tubes (TT) are used in clinical practice to connect an artificial ventilator to the patient's airways. It is important to know the pressure used to overcome tube impedance to avoid lung injury. Although high-frequency percussive ventilation (HFPV) has been increasingly used, the mechanical behavior of TT under HFPV has not yet been described. Thus, we aimed at characterizing in vitro the pressure drop across TT (ΔPTT) by identifying the model that best fits the measured pressure-flow (P-V̇) relationships during HFPV under different working pressures (PWork), percussive frequencies and mechanical loads. Three simple models relating ΔPTT and flow (V̇) were tested. Model 1 is characterized by linear resistive [Rtube ⋅ V̇(t)] and inertial [I · V̈(t)] terms. Model 2 takes into consideration Rohrer's approach [K1· V̇(t) + K2 ⋅V̇(t)] and inertance [I ·V̈(t)]. In model 3 the pressure drop caused by friction is represented by the non-linear Blasius component [Kb· V̇(1.75)(t)] and the inertial term [I· V̈(t)]. Model 1 presented a significantly higher root mean square error of approximation than models 2 and 3, which were similar. Thus, model 1 was not as accurate as the latter, possibly due to turbulence. Model 3 presented the most robust resistance-related coefficient. Estimated inertances did not vary among the models using the same tube. In conclusion, in HFPV ΔPTT can be easily calculated by the physician using model 3.


Asunto(s)
Ventilación de Alta Frecuencia , Intubación Intratraqueal , Presión , Tráquea , Hidrodinámica , Modelos Biológicos
2.
Rev Port Pneumol ; 20(1): 31-5, 2014.
Artículo en Inglés, Portugués | MEDLINE | ID: mdl-24315398

RESUMEN

This study aimed to investigate the association between respiratory mechanics and autonomic modulation in morbidly obese patients. We evaluated 10 morbidly obese subjects (BMI=52.9±11.2kg/m(2)), aged 23-58 years. Assessment of respiratory mechanics was done by the forced oscillation technique (FOT), and cardiovascular autonomic function was recorded by heart rate variability analysis (HRV). The Pearson correlation coefficient was used to test the associations between respiratory mechanics and HRV variables. There were associations between the standard deviation of all RR intervals (SDNN) and airway resistance (Rm) (r=-0.82; p=0.004), SDNN and respiratory system resistance (R0) (r=-0.79; p=0.006), root mean square of successive differences between adjacent normal RR intervals (rMSSD) and respiratory system resistance (R5) (r=-0.643; p=0.0451), rMSSD and R0 (r=-0.64; p=0.047), and rMSSD and Rm (r=-0.658; p=0.039). We concluded that the airway and respiratory system resistances are negatively associated with parasympathetic activity in patients with morbid obesity.


Asunto(s)
Frecuencia Cardíaca , Obesidad Mórbida/fisiopatología , Mecánica Respiratoria , Adulto , Sistema Nervioso Autónomo/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adulto Joven
3.
Inhal Toxicol ; 23(5): 257-67, 2011 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-21506876

RESUMEN

Air pollution is associated with morbidity and mortality induced by respiratory diseases. However, the mechanisms therein involved are not yet fully clarified. Thus, we tested the hypothesis that a single acute exposure to low doses of fine particulate matter (PM2.5) may induce functional and histological lung changes and unchain inflammatory and oxidative stress processes. PM2.5 was collected from the urban area of São Paulo city during 24 h and underwent analysis for elements and polycyclic aromatic hydrocarbon contents. Forty-six male BALB/c mice received intranasal instillation of 30 µL of saline (CTRL) or PM2.5 at 5 or 15 µg in 30 µL of saline (P5 and P15, respectively). Twenty-four hours later, lung mechanics were determined. Lungs were then prepared for histological and biochemical analysis. P15 group showed significantly increased lung impedance and alveolar collapse, as well as lung tissue inflammation, oxidative stress and damage. P5 presented values between CTRL and P15: higher mechanical impedance and inflammation than CTRL, but lower inflammation and oxidative stress than P15. In conclusion, acute exposure to low doses of fine PM induced lung inflammation, oxidative stress and worsened lung impedance and histology in a dose-dependent pattern in mice.


Asunto(s)
Lesión Pulmonar/inducido químicamente , Pulmón/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Material Particulado/toxicidad , Animales , Ciudades , Relación Dosis-Respuesta a Droga , Disulfuro de Glutatión/metabolismo , Pulmón/metabolismo , Pulmón/patología , Lesión Pulmonar/metabolismo , Lesión Pulmonar/fisiopatología , Masculino , Ratones , Ratones Endogámicos BALB C , Oxidorreductasas/metabolismo , Tamaño de la Partícula , Material Particulado/química , Pruebas de Función Respiratoria
4.
Respir Physiol Neurobiol ; 169(1): 62-8, 2009 Oct 31.
Artículo en Inglés | MEDLINE | ID: mdl-19712760

RESUMEN

We examined whether recruitment maneuvers (RMs) with gradual increase in airway pressure (RAMP) provide better outcome than continuous positive airway pressure (CPAP) in paraquat-induced acute lung injury (ALI). Wistar rats received saline intraperitoneally (0.5 mL, CTRL) or paraquat (15 mg/kg, ALI). Twenty-four hours later lung mechanics [static elastance, viscoelastic component of elastance, resistive, viscoelastic and total pressures] were determined before and after recruitment with 40cmH2O CPAP for 40s or 40-s-long slow increase in pressure up to 40cmH2O (RAMP) followed by 0 or 5 cmH2O PEEP. Fractional area of alveolar collapse and PCIII mRNA were determined. All mechanical parameters and the fraction area of alveolar collapse were higher in ALI compared to CTRL. Only RAMP-PEEP maneuver significantly improved lung mechanics and decreased PCIII mRNA expression (53%) compared with ALI, while both RMs followed by PEEP decreased alveolar collapse. In conclusion, in the present experimental ALI model, RAMP followed by 5cm H2O PEEP yields a better outcome.


Asunto(s)
Lesión Pulmonar Aguda/fisiopatología , Pulmón/patología , Respiración con Presión Positiva/métodos , Reclutamiento Neurofisiológico/fisiología , Mecánica Respiratoria/fisiología , Lesión Pulmonar Aguda/inducido químicamente , Lesión Pulmonar Aguda/metabolismo , Lesión Pulmonar Aguda/patología , Análisis de Varianza , Animales , Colágeno Tipo III/genética , Colágeno Tipo III/metabolismo , Modelos Animales de Enfermedad , Regulación de la Expresión Génica , Pulmón/metabolismo , Mediciones del Volumen Pulmonar , Paraquat , ARN Mensajero/metabolismo , Ratas , Ratas Wistar
5.
Respir Physiol Neurobiol ; 168(3): 203-9, 2009 Sep 30.
Artículo en Inglés | MEDLINE | ID: mdl-19573627

RESUMEN

This study investigated whether repeated administration of recombinant adeno-associated virus type 5 (rAAV5) to the airways induces inflammatory processes in the lungs of BALB/c-mice, with mechanical and histologic changes. Saline was instilled intratracheally in the control group, and rAAV5-green fluorescence protein (GFP) (4x10(11)particles) in the virus group (VR). These groups were subdivided into four subgroups: one dose analyzed 3 weeks later (VR1d3w) and two doses analyzed 1 (VR2d1w), 2 (VR2d2w) and 3 weeks (VR2d3w) after the second dose. Lung morphometry, mechanical parameters, airway responsiveness, rAAV5-GFP transduction and the expression of inflammatory cytokines were investigated. No significant differences in lung mechanics, airway responsiveness, and morphometry were observed. Re-administration of rAAV5 vector resulted in a decrease in GFP mRNA expression in the VR2d3w group. There was no evidence of inflammatory response or apoptosis in any group. rAAV5 did not induce an inflammatory process, mechanical or morphometric changes in the lungs. AAV5 may be an appropriate vector for lung gene therapy.


Asunto(s)
Terapia Genética/efectos adversos , Vectores Genéticos/efectos adversos , Neumonía/etiología , Neumonía/patología , Resistencia de las Vías Respiratorias , Análisis de Varianza , Animales , Apoptosis , Modelos Animales de Enfermedad , Proteínas Fluorescentes Verdes/genética , Etiquetado Corte-Fin in Situ , Masculino , Ratones , Ratones Endogámicos BALB C , ARN Mensajero/metabolismo , Mecánica Respiratoria/fisiología , Factores de Tiempo
6.
Eur Respir J ; 33(3): 634-45, 2009 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-19010991

RESUMEN

The present study compared the effects of early short-term with prolonged low-dose corticosteroid therapy in acute lung injury (ALI). In total, 120 BALB/c mice were randomly divided into five groups. In the control group, saline was intratracheally (i.t.) instilled. In the ALI group, mice received Escherichia coli lipopolysaccharide (10 microg i.t.). ALI animals were further randomised into four subgroups to receive saline (0.1 mL i.v.) or methylprednisolone (2 mg x kg(-1) i.v.) at 6 h, 24 h or daily (for 7 days, beginning at day 1). At 1, 3 and 8 weeks, in vivo and in vitro lung mechanics and histology (light and electron microscopy), collagen and elastic fibre content, cytokines in bronchoalveolar lavage fluid and the expression of matrix metalloproteinase (MMP)-9 and -2 were measured. In vivo (static elastance and viscoelastic pressure) and in vitro (tissue elastance and resistance) lung mechanics, alveolar collapse, cell infiltration, collagen and elastic fibre content and the expression of MMP-9 and MMP-2 were increased in ALI at 1 week. Methylprednisolone led to a complete resolution of lung mechanics, avoided fibroelastogenesis and the increase in the expression of MMP-9 and MMP-2 independent of steroid treatment design. Thus, early short-term, low-dose methylprednisolone is as effective as prolonged therapy in acute lung injury.


Asunto(s)
Lesión Pulmonar/tratamiento farmacológico , Lesión Pulmonar/patología , Metilprednisolona/administración & dosificación , Enfermedad Aguda , Animales , Antiinflamatorios/administración & dosificación , Colágeno/química , Citocinas/metabolismo , Escherichia coli/metabolismo , Inflamación , Lipopolisacáridos/metabolismo , Metaloproteinasa 2 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/metabolismo , Ratones , Ratones Endogámicos BALB C , Factores de Tiempo
7.
Respir Physiol Neurobiol ; 164(3): 331-7, 2008 Dec 31.
Artículo en Inglés | MEDLINE | ID: mdl-18782634

RESUMEN

We determined whether microcrystalline cellulose (MCC), a component of pharmaceutical tablets, induces pulmonary changes. In vivo [resistive and viscoelastic pressures (DeltaP(1) and DeltaP(2)), static elastance (E(L))] and in vitro [tissue resistance (R), elastance (E), and hysteresivity (eta)] lung mechanics, histology, and bronchoalveolar lavage fluid (BALF) were analyzed 3h, 24h, and 3, 15 and 30 days after intratracheal instillation of saline (C) or MCC in BALB/c mice. DeltaP(1) increased at 3h, remaining higher than C until day 3, while E(L) and DeltaP(2) increased only at 24h. At 3 days all mechanical parameters returned to baseline. R and E increased only at 24h. MCC increased alveolar collapse and the number of neutrophils in BALF at 3h, until 3 and 15 days, respectively. At 3 days MCC migrate from the airways into the parenchyma, where they were observed until 30 days. In conclusion, microcrystalline cellulose yielded an acute and self-limited inflammation that impaired lung mechanics.


Asunto(s)
Celulosa/efectos adversos , Excipientes/efectos adversos , Inflamación/inducido químicamente , Pulmón/patología , Pulmón/fisiopatología , Resistencia de las Vías Respiratorias/efectos de los fármacos , Resistencia de las Vías Respiratorias/fisiología , Animales , Líquido del Lavado Bronquioalveolar , Inflamación/fisiopatología , Modelos Lineales , Ratones , Ratones Endogámicos BALB C , Alveolos Pulmonares/patología , Atelectasia Pulmonar/inducido químicamente , Distribución Aleatoria , Mecánica Respiratoria , Factores de Tiempo
8.
Braz J Med Biol Res ; 39(6): 697-706, 2006 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-16751974

RESUMEN

Physical forces affect both the function and phenotype of cells in the lung. Bronchial, alveolar, and other parenchymal cells, as well as fibroblasts and macrophages, are normally subjected to a variety of passive and active mechanical forces associated with lung inflation and vascular perfusion as a result of the dynamic nature of lung function. These forces include changes in stress (force per unit area) or strain (any forced change in length in relation to the initial length) and shear stress (the stress component parallel to a given surface). The responses of cells to mechanical forces are the result of the cell's ability to sense and transduce these stimuli into intracellular signaling pathways able to communicate the information to its interior. This review will focus on the modulation of intracellular pathways by lung mechanical forces and the intercellular signaling. A better understanding of the mechanisms by which lung cells transduce physical forces into biochemical and biological signals is of key importance for identifying targets for the treatment and prevention of physical force-related disorders.


Asunto(s)
Pulmón/fisiología , Mecanorreceptores/fisiología , Mecanotransducción Celular/fisiología , Matriz Extracelular/fisiología , Humanos , Uniones Intercelulares/fisiología , Membranas Intracelulares/fisiología , Pulmón/citología , Estrés Mecánico
9.
Braz. j. med. biol. res ; 39(6): 697-706, June 2006. ilus
Artículo en Inglés | LILACS | ID: lil-428282

RESUMEN

Physical forces affect both the function and phenotype of cells in the lung. Bronchial, alveolar, and other parenchymal cells, as well as fibroblasts and macrophages, are normally subjected to a variety of passive and active mechanical forces associated with lung inflation and vascular perfusion as a result of the dynamic nature of lung function. These forces include changes in stress (force per unit area) or strain (any forced change in length in relation to the initial length) and shear stress (the stress component parallel to a given surface). The responses of cells to mechanical forces are the result of the cell's ability to sense and transduce these stimuli into intracellular signaling pathways able to communicate the information to its interior. This review will focus on the modulation of intracellular pathways by lung mechanical forces and the intercellular signaling. A better understanding of the mechanisms by which lung cells transduce physical forces into biochemical and biological signals is of key importance for identifying targets for the treatment and prevention of physical force-related disorders.


Asunto(s)
Humanos , Pulmón/fisiología , Mecanorreceptores/fisiología , Mecanotransducción Celular/fisiología , Matriz Extracelular/fisiología , Uniones Intercelulares/fisiología , Membranas Intracelulares/fisiología , Pulmón/citología , Estrés Mecánico
10.
Br J Anaesth ; 96(4): 533-6, 2006 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-16490764

RESUMEN

We report the case of a patient that had undergone a left pneumonectomy during which a double-lumen tube was used and an undetected right bronchial laceration occurred. After diagnosis the patient underwent a second operation to repair the tear. The role of high-frequency percussive ventilation in enabling adequate gas exchange during the bronchial repair is described and discussed.


Asunto(s)
Bronquios/cirugía , Ventilación de Alta Frecuencia/métodos , Neumonectomía/efectos adversos , Bronquios/lesiones , Dióxido de Carbono/sangre , Humanos , Cuidados Intraoperatorios/métodos , Intubación Intratraqueal/efectos adversos , Masculino , Persona de Mediana Edad , Oxígeno/sangre , Presión Parcial , Intercambio Gaseoso Pulmonar
11.
Braz J Med Biol Res ; 39(2): 283-7, 2006 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-16470317

RESUMEN

The aim of the present study was to compare the efficacy of a novel phosphodiesterase 4 and 5 inhibitor, LASSBio596, with that of dexamethasone in a murine model of chronic asthma. Lung mechanics (airway resistance, viscoelastic pressure, and static elastance), histology, and airway and lung parenchyma remodeling (quantitative analysis of collagen and elastic fiber) were analyzed. Thirty-three BALB/c mice were randomly assigned to four groups. In the asthma group (N = 9), mice were immunized with 10 microg ovalbumin (OVA, ip) on 7 alternate days, and after day 40 they were challenged with three intratracheal instillations of 20 microg OVA at 3-day intervals. Control mice (N = 8) received saline under the same protocol. In the dexamethasone (N = 8) and LASSBio596 (N = 8) groups, the animals of the asthma group were treated with 1 mg/kg dexamethasone disodium phosphate (0.1 mL, ip) or 10 mg/kg LASSBio596 dissolved in dimethyl sulfoxide (0.2 mL, ip) 24 h before the first intratracheal instillation of OVA, for 8 days. Airway resistance, viscoelastic pressure and static elastance increased significantly in the asthma group (77, 56, and 76%, respectively) compared to the control group. The asthma group presented more intense alveolar collapse, bronchoconstriction, and eosinophil and neutrophil infiltration than the control group. Both LASSBio596 and dexamethasone inhibited the changes in lung mechanics, tissue cellularity, bronchoconstriction, as well as airway and lung parenchyma remodeling. In conclusion, LASSBio596 at a dose of 10 mg/kg effectively prevented lung mechanical and morphometrical changes and had the potential to block fibroproliferation in a BALB/c mouse model of asthma.


Asunto(s)
Asma/tratamiento farmacológico , Inhibidores de Fosfodiesterasa/farmacología , Ftalimidas/farmacología , Mecánica Respiratoria/efectos de los fármacos , Animales , Asma/patología , Enfermedad Crónica , Dexametasona/farmacología , Modelos Animales de Enfermedad , Ratones , Ratones Endogámicos BALB C , Ácidos Ftálicos , Distribución Aleatoria , Pruebas de Función Respiratoria , Sulfonamidas
12.
Respir Physiol Neurobiol ; 150(1): 44-51, 2006 Jan 25.
Artículo en Inglés | MEDLINE | ID: mdl-16448933

RESUMEN

High-frequency percussive ventilation (HFPV) has been proved useful in patients with acute respiratory distress syndrome. However, its physiological mechanisms are still poorly understood. The aim of this work is to evaluate the effects of mechanical loading on the tidal volume and lung washout during HFPV. For this purpose a single-compartment mechanical lung simulator, which allows the combination of three elastic and four resistive loads (E and R, respectively), underwent HFPV with constant ventilator settings. With increasing E and decreasing R the tidal volume/cumulative oscillated gas volume ratio fell, while the duration of end-inspiratory plateau/inspiratory time increased. Indeed, an inverse linear relationship was found between these two ratios. Peak and mean pressure in the model decreased linearly with increasing pulsatile volume, the latter to a lesser extent. In conclusion, elastic or resistive loading modulates the mechanical characteristics of the HFPV device but in such a way that washout volume and time allowed for diffusive ventilation vary agonistically.


Asunto(s)
Resistencia de las Vías Respiratorias/fisiología , Ventilación de Alta Frecuencia/métodos , Pulmón/fisiología , Volumen de Ventilación Pulmonar/fisiología , Simulación por Computador , Humanos , Modelos Lineales , Mediciones del Volumen Pulmonar/métodos , Ventilación Pulmonar/fisiología , Factores de Tiempo
13.
Braz. j. med. biol. res ; 39(2): 283-287, Feb. 2006. tab
Artículo en Inglés | LILACS | ID: lil-420281

RESUMEN

The aim of the present study was to compare the efficacy of a novel phosphodiesterase 4 and 5 inhibitor, LASSBio596, with that of dexamethasone in a murine model of chronic asthma. Lung mechanics (airway resistance, viscoelastic pressure, and static elastance), histology, and airway and lung parenchyma remodeling (quantitative analysis of collagen and elastic fiber) were analyzed. Thirty-three BALB/c mice were randomly assigned to four groups. In the asthma group (N = 9), mice were immunized with 10 æg ovalbumin (OVA, ip) on 7 alternate days, and after day 40 they were challenged with three intratracheal instillations of 20 æg OVA at 3-day intervals. Control mice (N = 8) received saline under the same protocol. In the dexamethasone (N = 8) and LASSBio596 (N = 8) groups, the animals of the asthma group were treated with 1 mg/kg dexamethasone disodium phosphate (0.1 mL, ip) or 10 mg/kg LASSBio596 dissolved in dimethyl sulfoxide (0.2 mL, ip) 24 h before the first intratracheal instillation of OVA, for 8 days. Airway resistance, viscoelastic pressure and static elastance increased significantly in the asthma group (77, 56, and 76 percent, respectively) compared to the control group. The asthma group presented more intense alveolar collapse, bronchoconstriction, and eosinophil and neutrophil infiltration than the control group. Both LASSBio596 and dexamethasone inhibited the changes in lung mechanics, tissue cellularity, bronchoconstriction, as well as airway and lung parenchyma remodeling. In conclusion, LASSBio596 at a dose of 10 mg/kg effectively prevented lung mechanical and morphometrical changes and had the potential to block fibroproliferation in a BALB/c mouse model of asthma.


Asunto(s)
Animales , Ratones , Asma/tratamiento farmacológico , Inhibidores de Fosfodiesterasa/farmacología , Ftalimidas/farmacología , Mecánica Respiratoria/efectos de los fármacos , Asma/patología , Enfermedad Crónica , Modelos Animales de Enfermedad , Dexametasona/farmacología , Ratones Endogámicos BALB C , Distribución Aleatoria , Pruebas de Función Respiratoria
14.
Braz J Med Biol Res ; 38(2): 147-59, 2005 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-15785826

RESUMEN

Improving the course and outcome of patients with acute respiratory distress syndrome presents a challenge. By understanding the immune status of a patient, physicians can consider manipulating proinflammatory systems more rationally. In this context, corticosteroids could be a therapeutic tool in the armamentarium against acute respiratory distress syndrome. Corticosteroid therapy has been studied in three situations: prevention in high-risk patients, early treatment with high-dose, short-course therapy, and prolonged therapy in unresolving cases. There are differences between the corticosteroid trials of the past and recent trials: today, treatment starts 2-10 days after disease onset in patients that failed to improve; in the past, the corticosteroid doses employed were 5-140 times higher than those used now. Additionally, in the past treatment consisted of administering one to four doses every 6 h (methylprednisolone, 30 mg/kg) versus prolonging treatment as long as necessary in the new trials (2 mg kg(-1) day(-1) every 6 h). The variable response to corticosteroid treatment could be attributed to the heterogeneous biochemical and molecular mechanisms activated in response to different initial insults. Numerous factors need to be taken into account when corticosteroids are used to treat acute respiratory distress syndrome: the specificity of inhibition, the duration and degree of inhibition, and the timing of inhibition. The major continuing problem is when to administer corticosteroids and how to monitor their use. The inflammatory mechanisms are continuous and cyclic, sometimes causing deterioration or improvement of lung function. This article reviews the mechanisms of action of corticosteroids and the results of experimental and clinical studies regarding the use of corticosteroids in acute respiratory distress syndrome.


Asunto(s)
Corticoesteroides/uso terapéutico , Glucocorticoides/uso terapéutico , Síndrome de Dificultad Respiratoria/tratamiento farmacológico , Animales , Ensayos Clínicos como Asunto , Humanos , Síndrome de Dificultad Respiratoria/prevención & control
15.
Braz. j. med. biol. res ; 38(2): 147-159, fev. 2005. ilus, tab
Artículo en Inglés | LILACS | ID: lil-393657

RESUMEN

Improving the course and outcome of patients with acute respiratory distress syndrome presents a challenge. By understanding the immune status of a patient, physicians can consider manipulating proinflammatory systems more rationally. In this context, corticosteroids could be a therapeutic tool in the armamentarium against acute respiratory distress syndrome. Corticosteroid therapy has been studied in three situations: prevention in high-risk patients, early treatment with high-dose, short-course therapy, and prolonged therapy in unresolving cases. There are differences between the corticosteroid trials of the past and recent trials: today, treatment starts 2-10 days after disease onset in patients that failed to improve; in the past, the corticosteroid doses employed were 5-140 times higher than those used now. Additionally, in the past treatment consisted of administering one to four doses every 6 h (methylprednisolone, 30 mg/kg) versus prolonging treatment as long as necessary in the new trials (2 mg kg-1 day-1 every 6 h). The variable response to corticosteroid treatment could be attributed to the heterogeneous biochemical and molecular mechanisms activated in response to different initial insults. Numerous factors need to be taken into account when corticosteroids are used to treat acute respiratory distress syndrome: the specificity of inhibition, the duration and degree of inhibition, and the timing of inhibition. The major continuing problem is when to administer corticosteroids and how to monitor their use. The inflammatory mechanisms are continuous and cyclic, sometimes causing deterioration or improvement of lung function. This article reviews the mechanisms of action of corticosteroids and the results of experimental and clinical studies regarding the use of corticosteroids in acute respiratory distress syndrome.


Asunto(s)
Humanos , Animales , Corticoesteroides/uso terapéutico , Glucocorticoides/uso terapéutico , Síndrome de Dificultad Respiratoria/tratamiento farmacológico , Ensayos Clínicos como Asunto , Síndrome de Dificultad Respiratoria/prevención & control
16.
J Cell Mol Med ; 8(3): 285-93, 2004.
Artículo en Inglés | MEDLINE | ID: mdl-15491504

RESUMEN

Following inflammation and injury in the lung, loss of epithelial cell precursors could determine the balance between tissue regeneration and fibrosis. This review discusses evidence that proapoptotic Fas-Fas ligand (FasL) signaling plays a central role in pulmonary inflammation, injury and fibrosis. FasL signaling induces inflammatory apoptosis in epithelial cells and alveolar macrophages, with concomitant IL-1 beta and chemokine release, leading to neutrophil infiltration. FasL signaling plays a critical role in models of acute lung injury, idiopathic pulmonary fibrosis and silicosis; blockade of Fas-FasL interactions either prevents or attenuates pulmonary inflammation and fibrosis. Serologic and immunohistochemical studies in patients support a major pathogenic role of Fas and FasL molecules in inflammatory lung diseases. Identification of the pathogenic role of FasL could facilitate the discovery of more effective treatments for currently untreatable inflammatory lung diseases.


Asunto(s)
Glicoproteínas de Membrana/fisiología , Neumonía/inmunología , Receptor fas/inmunología , Enfermedad Aguda , Apoptosis , Células Epiteliales/metabolismo , Células Epiteliales/patología , Proteína Ligando Fas , Regulación de la Expresión Génica , Humanos , Interleucina-1/metabolismo , Macrófagos Alveolares/inmunología , Macrófagos Alveolares/patología , Neutrófilos/inmunología , Neumonía/metabolismo , Alveolos Pulmonares/inmunología , Alveolos Pulmonares/metabolismo , Fibrosis Pulmonar/inmunología , Fibrosis Pulmonar/metabolismo , Transducción de Señal , Silicosis/inmunología
17.
Respir Physiol Neurobiol ; 142(1): 81-91, 2004 Aug 20.
Artículo en Inglés | MEDLINE | ID: mdl-15351306

RESUMEN

High-frequency percussive ventilation (HFPV) has proved its unique efficacy in the treatment of acute respiratory distress, when conventional mechanical ventilation (CMV) has demonstrated a limited response. We analysed flow (V(dot)), volume (V) and airway pressure (Paw) during ventilation of a single-compartment mechanical lung simulator, in which resistance (R) and elastance (E) values were modified, while maintaining the selected ventilatory settings of the HFPV device. These signals reveal the physical effect of the imposed loads on the output of the ventilatory device, secondary to constant (millisecond by millisecond) alterations in pulmonary dynamics. V(dot), V and Paw values depended fundamentally on the value of R, but their shapes were modified by R and E. Although peak Paw increased 70.3% in relation to control value, mean Paw augmented solely 36.5% under the same circumstances (maximum of 9.4 cm H2O). Finally, a mechanism for washing gas out of the lung was suggested.


Asunto(s)
Resistencia de las Vías Respiratorias/fisiología , Ventilación de Alta Frecuencia/métodos , Pulmón/fisiología , Ventilación Pulmonar/fisiología , Respiración , Volumen de Ventilación Pulmonar/fisiología , Humanos , Mediciones del Volumen Pulmonar , Respiración Artificial
18.
Braz. j. med. biol. res ; 37(8): 1225-1229, Aug. 2004. ilus, graf
Artículo en Inglés | LILACS | ID: lil-362561

RESUMEN

Toxic cyanobacteria in drinking water supplies can cause serious public health problems. In the present study we analyzed the time course of changes in lung histology in young and adult male Swiss mice injected intraperitoneally (ip) with a cyanobacterial extract containing the hepatotoxic microcystins. Microcystins are cyclical heptapeptides quantified by ELISA method. Ninety mice were divided into two groups. Group C received an injection of saline (300 µl, ip) and group Ci received a sublethal dose of microcystins (48.2 µg/kg, ip). Mice of the Ci group were further divided into young (4 weeks old) and adult (12 weeks old) animals. At 2 and 8 h and at 1, 2, 3, and 4 days after the injection of the toxic cyanobacterial extract, the mice were anesthetized and the trachea was occluded at end-expiration. The lungs were removed en bloc, fixed, sectioned, and stained with hematoxylin-eosin. The percentage of the area of alveolar collapse and the number of polymorphonuclear (PMN) and mononuclear cell infiltrations were determined by point counting. Alveolar collapse increased from C to all Ci groups (123 to 262 percent) independently of time, reaching a maximum value earlier in young than in adult animals. The amount of PMN cells increased with time of the lesion (52 to 161 percent). The inflammatory response also reached the highest level earlier in young than in adult mice. After 2 days, PMN levels remained unchanged in adult mice, while in young mice the maximum number was observed at day 1 and was similar at days 2, 3, and 4. We conclude that the toxins and/or other cyanobacterial compounds probably exert these effects by reaching the lung through the blood stream after ip injection.


Asunto(s)
Animales , Masculino , Ratones , Toxinas Bacterianas , Cianobacterias , Inhibidores Enzimáticos , Pulmón
19.
Braz J Med Biol Res ; 37(8): 1225-9, 2004 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-15273824

RESUMEN

Toxic cyanobacteria in drinking water supplies can cause serious public health problems. In the present study we analyzed the time course of changes in lung histology in young and adult male Swiss mice injected intraperitoneally (ip) with a cyanobacterial extract containing the hepatotoxic microcystins. Microcystins are cyclical heptapeptides quantified by ELISA method. Ninety mice were divided into two groups. Group C received an injection of saline (300 microl, ip) and group Ci received a sublethal dose of microcystins (48.2 microg/kg, ip). Mice of the Ci group were further divided into young (4 weeks old) and adult (12 weeks old) animals. At 2 and 8 h and at 1, 2, 3, and 4 days after the injection of the toxic cyanobacterial extract, the mice were anesthetized and the trachea was occluded at end-expiration. The lungs were removed en bloc, fixed, sectioned, and stained with hematoxylin-eosin. The percentage of the area of alveolar collapse and the number of polymorphonuclear (PMN) and mononuclear cell infiltrations were determined by point counting. Alveolar collapse increased from C to all Ci groups (123 to 262%) independently of time, reaching a maximum value earlier in young than in adult animals. The amount of PMN cells increased with time of the lesion (52 to 161%). The inflammatory response also reached the highest level earlier in young than in adult mice. After 2 days, PMN levels remained unchanged in adult mice, while in young mice the maximum number was observed at day 1 and was similar at days 2, 3, and 4. We conclude that the toxins and/or other cyanobacterial compounds probably exert these effects by reaching the lung through the blood stream after ip injection.


Asunto(s)
Toxinas Bacterianas/toxicidad , Cianobacterias/química , Inhibidores Enzimáticos/toxicidad , Pulmón/efectos de los fármacos , Péptidos Cíclicos/toxicidad , Animales , Toxinas Bacterianas/aislamiento & purificación , Inhibidores Enzimáticos/aislamiento & purificación , Pulmón/patología , Masculino , Ratones , Microcistinas , Péptidos Cíclicos/aislamiento & purificación
20.
Respir Physiol Neurobiol ; 139(3): 271-80, 2004 Feb 25.
Artículo en Inglés | MEDLINE | ID: mdl-15122993

RESUMEN

The aim of this study was to determine whether an intrapleural injection of barium sulphate would produce pleurodesis in rats. Additionally, respiratory mechanics and pleural remodelling were analysed. Single intrapleural injection of barium sulphate (100%) or saline was given to Wistar rats. Respiratory system, lung, and chest wall elastic, resistive and viscoelastic/inhomogeneous pressures were measured by the end-inflation occlusion method at 2 and 30 days after injection. The pleura were examined for gross and histopathological evidence of pleural inflammation and fibrosis, and the underlying lungs were also studied by morphometry. All pulmonary mechanical parameters increased at day 2, but were not different from control at 30 days after injection. Chest wall mechanical parameters did not change. Macroscopic evaluation demonstrated pleural adherence without haemothorax. Histopathologic analysis showed pleural inflammation and fibrosis. There was no alveolar inflammation or fibrosis in both groups. In conclusion, barium sulphate induced pleurodesis with either no changes in respiratory mechanics or lung lesion at day 30.


Asunto(s)
Sulfato de Bario/farmacología , Pleura/efectos de los fármacos , Pleurodesia , Mecánica Respiratoria/efectos de los fármacos , Animales , Fibrosis/etiología , Capacidad Residual Funcional/efectos de los fármacos , Histología , Inflamación/etiología , Rendimiento Pulmonar/efectos de los fármacos , Masculino , Pleura/patología , Pleura/fisiología , Ratas , Ratas Wistar , Mecánica Respiratoria/fisiología , Sistema Respiratorio/efectos de los fármacos , Tórax/efectos de los fármacos , Tórax/patología , Factores de Tiempo
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