RESUMO
BACKGROUND: Hyperinflation has been associated with negative cardiocirculatory consequences in patients with chronic obstructive pulmonary disease (COPD). These abnormalities are likely to worsen when the demands for O2 increase, e.g., under the stress of exercise. Thus, pharmacologically-induced lung deflation may improve cardiopulmonary interactions and exertional cardiac output leading to higher limb muscle blood flow and oxygenation in hyperinflated patients with COPD. METHODS: 20 patients (residual volumeâ¯=â¯201.6⯱â¯63.6% predicted) performed endurance cardiopulmonary exercise tests (75% peak) 1â¯h after placebo or tiotropium/olodaterol 5/5⯵g via the Respimat® inhaler (Boehringer Ingelheim, Ingelheim am Rhein, Germany). Cardiac output was assessed by signal-morphology impedance cardiography. Near-infrared spectroscopy determined quadriceps blood flow (indocyanine green dye) and intra-muscular oxygenation. RESULTS: Tiotropium/olodaterol was associated with marked lung deflation (pâ¯<â¯0.01): residual volume decreased by at least 0.4â¯L in 14/20 patients (70%). The downward shift in the resting static lung volumes was associated with less exertional inspiratory constraints and dyspnoea thereby increasing exercise endurance by ~50%. Contrary to our premises, however, neither central and peripheral hemodynamics nor muscle oxygenation improved after active intervention compared to placebo. These results were consistent with those found in a subgroup of patients showing the largest decrements in residual volume (pâ¯<â¯0.05). CONCLUSIONS: The beneficial effects of tiotropium/olodaterol on resting and operating lung volumes are not translated into enhanced cardiocirculatory responses to exertion in hyperinflated patients with COPD. Improvement in exercise tolerance after dual bronchodilation is unlikely to be mechanistically linked to higher muscle blood flow and/or O2 delivery.
Assuntos
Benzoxazinas/efeitos adversos , Broncodilatadores/efeitos adversos , Débito Cardíaco/efeitos dos fármacos , Atelectasia Pulmonar/induzido quimicamente , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Brometo de Tiotrópio/efeitos adversos , Idoso , Idoso de 80 Anos ou mais , Benzoxazinas/administração & dosagem , Benzoxazinas/uso terapêutico , Broncodilatadores/administração & dosagem , Broncodilatadores/uso terapêutico , Estudos de Casos e Controles , Estudos Cross-Over , Estudos Transversais , Combinação de Medicamentos , Dispneia/fisiopatologia , Teste de Esforço/métodos , Tolerância ao Exercício/efeitos dos fármacos , Feminino , Hemodinâmica/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Nebulizadores e Vaporizadores , Oxigênio/metabolismo , Esforço Físico/efeitos dos fármacos , Placebos/administração & dosagem , Músculo Quadríceps/irrigação sanguínea , Músculo Quadríceps/diagnóstico por imagem , Músculo Quadríceps/metabolismo , Fluxo Sanguíneo Regional/efeitos dos fármacos , Volume Residual/efeitos dos fármacos , Espectroscopia de Luz Próxima ao Infravermelho/métodos , Brometo de Tiotrópio/administração & dosagem , Brometo de Tiotrópio/uso terapêuticoRESUMO
PURPOSE: To analyze microscopically the effects of different concentrations of oxygen in the lungs of rats. METHODS: There were 20 rats distributed in three experimental groups (concentration of oxygen to 40%, 70% and 100%) and a control group. The animals were exposed to the oxygen in a chamber of acrylic during three days and after exposition, the animals were submitted to median thoracotomia to remove the lungs. The lung tissue of all of the animals was analyzed as regards presence of acute and chronic inflammation, capillary congestion, alveolar walls thick, interstitial and alveolar edema, alveolar hemorrhage, denudation capillary and alveolar endothelium areas and atelectasis. RESULTS: The analysis histopathologic revealed significant statistics difference for acute and chronic inflammation, capillary congestion, alveolar walls thick, interstitial and alveolar edema, alveolar hemorrhage, denudation capillary and alveolar epithelium areas. CONCLUSIONS: Exposition to the oxygen during 72 hours in the concentration of 40% does not produce significant histopathologic alterations in the lung tissue; in the concentration of 70%, can promotes the alveolar walls thick and capillary congestion and in the concentration of 100% can cause death and originate diffuse pulmonary lesion.
Assuntos
Pulmão/patologia , Oxigênio/efeitos adversos , Alvéolos Pulmonares/patologia , Animais , Feminino , Hiperemia/induzido quimicamente , Modelos Animais , Oxigênio/toxicidade , Pneumonia/induzido quimicamente , Alvéolos Pulmonares/lesões , Atelectasia Pulmonar/induzido quimicamente , Distribuição Aleatória , Ratos Wistar , Fatores de TempoRESUMO
PURPOSE: To analyze microscopically the effects of different concentrations of oxygen in the lungs of rats. METHODS: There were 20 rats distributed in three experimental groups (concentration of oxygen to 40%, 70% and 100%) and a control group. The animals were exposed to the oxygen in a chamber of acrylic during three days and after exposition, the animals were submitted to median thoracotomia to remove the lungs. The lung tissue of all of the animals was analyzed as regards presence of acute and chronic inflammation, capillary congestion, alveolar walls thick, interstitial and alveolar edema, alveolar hemorrhage, denudation capillary and alveolar endothelium areas and atelectasis. RESULTS: The analysis histopathologic revealed significant statistics difference for acute and chronic inflammation, capillary congestion, alveolar walls thick, interstitial and alveolar edema, alveolar hemorrhage, denudation capillary and alveolar epithelium areas. CONCLUSIONS: Exposition to the oxygen during 72 hours in the concentration of 40% does not produce significant histopathologic alterations in the lung tissue; in the concentration of 70%, can promotes the alveolar walls thick and capillary congestion and in the concentration of 100% can cause death and originate diffuse pulmonary lesion. .
Assuntos
Animais , Feminino , Oxigênio/efeitos adversos , Alvéolos Pulmonares/patologia , Pulmão/patologia , Oxigênio/toxicidade , Pneumonia/induzido quimicamente , Alvéolos Pulmonares/lesões , Atelectasia Pulmonar/induzido quimicamente , Fatores de Tempo , Distribuição Aleatória , Ratos Wistar , Modelos Animais , Hiperemia/induzido quimicamenteRESUMO
General anesthesia is frequently associated to transient hypoxemia and lung atelectasis. Although volatile anesthetics are safe and widely used, their potential role on anesthesia-induced pulmonary impairment has not been fully explored. In this study, we investigated the effect of volatile anesthetic sevoflurane on pulmonary surfactant composition and structure that could contribute to atelectasis. After 30 min of sevoflurane anesthesia, Sprague-Dawley rats showed increased levels of lyso-phosphatidylcholine and decreased levels of phosphatidylcholine associated with significant impairment in lung mechanics and alveolar collapse, but showed no deterioration of alveolar fluid reabsorption when compared to control group of rats anesthetized with pentobarbital. Exposure to sevoflurane altered the thermotropic profile of surfactant model membranes, as detected by fluorescence anisotropy. In this sense, sevoflurane-promoted fluidification of condensed phases could potentially impair the ability of surfactant films to sustain the lowest surface tensions. In conclusion, the observed changes in surfactant composition and viscosity properties suggest a direct effect of sevoflurane on surfactant function, a factor potentially involved in anesthetic-induced alterations in lung mechanics.
Assuntos
Anestésicos Inalatórios/toxicidade , Éteres Metílicos/toxicidade , Alvéolos Pulmonares/efeitos dos fármacos , Surfactantes Pulmonares/metabolismo , Animais , Polarização de Fluorescência , Lisofosfatidilcolinas/metabolismo , Masculino , Fosfatidilcolinas/metabolismo , Alvéolos Pulmonares/patologia , Atelectasia Pulmonar/induzido quimicamente , Ratos , Ratos Sprague-Dawley , Sevoflurano , Tensão Superficial/efeitos dos fármacos , Viscosidade/efeitos dos fármacosRESUMO
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.
Assuntos
Celulose/efeitos adversos , Excipientes/efeitos adversos , Inflamação/induzido quimicamente , Pulmão/patologia , Pulmão/fisiopatologia , Resistência das Vias Respiratórias/efeitos dos fármacos , Resistência das Vias Respiratórias/fisiologia , Animais , Líquido da Lavagem Broncoalveolar , Inflamação/fisiopatologia , Modelos Lineares , Camundongos , Camundongos Endogâmicos BALB C , Alvéolos Pulmonares/patologia , Atelectasia Pulmonar/induzido quimicamente , Distribuição Aleatória , Mecânica Respiratória , Fatores de TempoRESUMO
Se intenta identificar los factores de riesgo relacionados con las complicaciones y anestesia utilizada en pacientes con cuerpos extraños en vía aérea y en esófago. Para ellos se realizó un protocolo recolectando antecedentes clínicos y epidemiológicos durante tres años consecutivos, con un total de 102 fichas clínicas de pacientes con sospecha o diagnóstico confirmado de esta emergencia. De estos, 60 se localizaban en esófago y 42, en vía aérea. Se analizaron los resultados, haciendo énfasis respecto a la elección de la inducción anestésica empleada en ambos grupos por separados y su relacion con las complicaciones encontradas. Se pesquisó un mayor porcentaje de complicaciones de origen respiratorio, en pacientes con cuerpos extraños en vía aérea, al utilizar inducción de tipo endovenosa en comparación con la inducción inhalatoria
Assuntos
Humanos , Anestesia Intravenosa/estatística & dados numéricos , Anestesia por Inalação/estatística & dados numéricos , Corpos Estranhos/cirurgia , Atelectasia Pulmonar/induzido quimicamente , Espasmo Brônquico/induzido quimicamente , Broncoscopia , Esofagoscopia , Anestesia Intravenosa/efeitos adversos , Anestesia por Inalação/efeitos adversos , Corpos Estranhos/complicações , Esôfago , Pneumotórax/induzido quimicamente , Obstrução das Vias Respiratórias/etiologiaRESUMO
Con el objetivo de conocer si la hidralazina (H) es capaz de inhibir la vasoconstricción hipóxica (VCH) se estudio su efecto sobre el cortocircuito intrapulmonar (Qs) en el modelo experimental de otelectasia regional (A). Se analizaron en siete perros los cambios circulatorios pulmonares y los del intercambio gaseoso en las siguientes condiciones: de control 1 (A y VCH), durante aumentos de flujo pulmonar alcanzando con la apertura de fístulas arteriovenosas (FA) (maniobra mecánica) y con el cierre de las mismas )control 2), después de la administración de hidralazina (0.33 mg/kg) y en el status y post sangrado controlado )control 3). Con la maniobra de FA se obtuvo un incremento significativo del gasto cardiaco (2.07 ñ 28 a 3.9 ñ 52 l. min, p <0.05), del Qs (de 13 ñ 1 a 23 ñ 3%, p <0.05) y de la pVO2 (38 ñ 2 a 48 ñ 1 mmHg p <0.05) con disminución en las resistencias pulmonares y sistémicas (Rs). Alcerrar las fístulas (C2) se alcanzó un estadio cardiopulmonar de equilibrio similar al de C1. Con el uso de H (intervención farmacológica) se observó en dirección y magnitud un cambio similar en el Qt (2.18 ñ 0.27 a 3.43 ñ 48 l. min. p <0.05); el Qs (14 ñ 1 a 23 ñ 3% p <0.05) y la pVO2: (40 ñ 2 a 48 ñ 3%, p <0.05) que con la maniobra mecánica de FA. Concluímos que la H es capaz de liberar la VCH pulmonar y que su mecanismo esta vinculado a las modificaciones de la pVO2 sin poder excluir su efecto farmacológico directo sobre la vasculatura pulmonar