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Epidemiological studies found that increases in the concentrations of airborne particulate matter (PM) smaller than 10 microns diameter (PM10) in the ambient air due to desert dust outbreaks contribute to global burden of diseases, primarily as a result of increased risk of cardiovascular morbidity and mortality. No studies have investigated the possible association between desert dust inhalation and airway inflammation in patients with ischemic heart disease (IHD). Induced sputum was collected in 38 patients and analysed to determine markers of airway inflammation (Transforming Growth Factor-β1 [TGF-β1] and hydroxyproline) concentrations. For the purpose of the investigation, PM10 and reactive gases concentrations measured in the European Air Quality Network implemented in the Canary Islands were also used. We identified Saharan desert dust using meteorology and dust models. Patients affected by smoking, chronic obstructive pulmonary disease (COPD), asthma, pulmonary abnormalities, acute bronchial or pulmonary disease were excluded. The median of age of patients was 64.71 years (56.35–71.54) and 14 (38.84%) of them were women. TGF-β1 and hydroxyproline in sputum were highly associated to PM10 inhalation from the Saharan desert. According to a regression model, an increase of 1 µg/m3 of PM10 concentrations due to desert dust, results in an increase of 3.84 pg/gwt of TGF-β1 (R2 adjusted= 89.69%) and of 0.80 μg/gwt of hydroxyproline (R2 adjusted= 85.28%) in the sputum of patients. The results of this study indicate that the exposure to high PM10 concentrations due to Saharan dust events are associated with intense inflammatory reaction in the airway mucosae of IHD-patients.

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Objetivo: El sulfato de magnesio (SM) ha demostrado tener en el asma bronquial un efecto broncodilatador, que resulta dudoso en el caso de la enfermedad pulmonar obstructiva cronica (EPOC). Por ello hemos llevado a cabo un estudio con el objetivo de investigar el posible efecto broncodilatador del SM intravenoso en la EPOC agudizada. Pacientes y metodos: Se estudio a 24 pacientes diagnosticados de EPOC agudizada que requirieron ingreso en la Unidad de Hospitalizacion de Neumologia. A cada uno se le realizo una espirometria basal. Posteriormente, se efectuo una aleatorizacion a doble ciego y cruzada de los pacientes para recibir 1,5 g de SM o placebo en solucion intravenosa (20 min). A quienes el primer dia recibieron SM se les administro placebo el segundo dia, y al reves. Se realizaron espirometrias a los 15, 30 y 45 min de la administracion de SM o placebo. Por ultimo, se administraron 400 µg de salbutamol inhalados mediante camara espaciadora y a los 15 min se realizo una ultima espirometria. Todos los enfermos recibieron ademas tratamiento con esteroides, antibioticos intravenosos, oxigeno y broncodilatadores pautados (salbutamol y bromuro de ipratropio cada 6 h). Resultados: Cuando se compararon los incrementos absolutos (en ml) y porcentuales del volumen espiratorio forzado en el primer segundo (FEV1) obtenidos con SM y placebo a los 15, 30 y 45 min, no se encontraron diferencias significativas. Al comparar los incrementos absolutos y porcentuales del FEV1 tras la administracion de salbutamol se observaron incrementos significativos con el SM (incrementos absolutos FEV1 SM/placebo: 0,185 ± 0,42 frente a 0,081 ± 0,01 l; p = 0,004. Incrementos porcentuales FEV1 SM/placebo: 17,11 ± 3,7% frente al 7,06 ± 1,8%; p = 0,008). Conclusiones: La administracion de SM intravenoso carece de efecto broncodilatador en pacientes con EPOC agudizada; sin embargo, si potencia dicho efecto de los betamimeticos inhalados.

Objective Magnesium sulfate has been shown to have a bronchodilating effect in asthma, but this effect has not been clearly established in the context of chronic obstructive pulmonary disease (COPD). For this reason we investigated the possible bronchodilating effect of magnesium sulfate in COPD exacerbations. Patients and methods We studied 24 patients with exacerbated COPD who required admission to our hospital's pneumology department. All patients underwent baseline spirometry and were subsequently randomized to groups in a double-blind crossover design. Patients received 1.5 g of magnesium sulfate or placebo in an intravenous solution for 20 minutes. Those who received magnesium sulfate the first day were given placebo the second day, and vice versa. Spirometry was performed 15, 30, and 45 minutes after administration of magnesium sulfate or placebo. Finally, 400 μg of salbutamol were administered using a spacer and a final spirometry was performed 15 minutes later. All patients also received treatment with corticosteroids, intravenous antibiotics, oxygen, and regularly-scheduled bronchodilator therapy (salbutamol and ipratropium bromide every 6 hours). Results When we compared absolute increase in liters and percentage increase in forced expiratory volume in 1 second (FEV1) obtained with magnesium sulfate application to the increases obtained with placebo after 15, 30, and 45 minutes, no significant differences were found. When we compared absolute and percentage increases in FEV1 after administering salbutamol, we found significantly greater increases after magnesium sulfate administration. The mean (SD) absolute increase in FEV1 was 0.185 (0.42) L after magnesium sulfate administration and 0.081 (0.01) L after placebo (P=.004). The percentage increase in FEV1 was 17.11% (3.7%) after magnesium sulfate and 7.06% (1.8%) after placebo (P=.008). Conclusions Intravenous administration of magnesium sulfate has no bronchodilating effect in patients with COPD exacerbations. It does, however, enhance the bronchodilating effect of inhaled β2-agonists.