American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Nov 1999
ReviewInduced sputum, eosinophilic bronchitis, and chronic obstructive pulmonary disease.
The application of sputum induction and refined methods of sputum examination has provided the opportunity to examine cell and molecular markers of airway inflammation in asthma, COPD, and other airway diseases. The measurements are relatively noninvasive and can be applied safely, with care, even in more severe exacerbations of asthma and severe COPD. Induced sputum examination can be applied at random and repeatedly and gives results that are reproducible, valid, and responsive to changes in treatment. ⋯ In contrast, there is increasing evidence that an absence of sputum eosinophilia is associated with steroid resistance. Hargreave FE, Leigh R. Induced sputum, eosinophilic bronchitis, and chronic obstructive pulmonary disease.
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Am. J. Respir. Crit. Care Med. · Nov 1999
Randomized Controlled Trial Comparative Study Clinical TrialDry powder versus intravenous and nebulized gentamicin in cystic fibrosis and bronchiectasis. A pilot study.
Aminoglycosides are a mainstay of therapy for patients with cystic fibrosis (CF) or non-CF bronchiectasis who are infected with Pseudomonas aeruginosa (Psa). Traditionally, aerosolized antibiotics are delivered by liquid nebulization. The objective of this study was to determine whether a gentamicin dry powder inhaler (DPI) is as microbiologically active and potentially safe as gentamicin inhaled via a small-volume nebulizer (SVN) or given intravenously. ⋯ No significant decline in bacterial counts was observed after intravenous gentamicin. When gentamicin was inhaled, blood concentrations were minimal, and were below concentrations known to cause systemic toxicity. For treatment of Psa infections susceptible to gentamicin, gentamicin administration by DPI appeared to be as efficient as by SVN, despite the delivery of a 7-fold lower dose to the airways.
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Am. J. Respir. Crit. Care Med. · Nov 1999
ReviewAirway inflammation in chronic obstructive pulmonary disease.
Cigarette smoking causes an inflammatory process in the central airways, peripheral airways, and lung parenchyma, even in smokers with normal lung function. The characteristics of this inflammatory process differ between smokers who develop chronic airflow limitation (COPD) and those who do not develop chronic airflow limitation: there is an increased infiltration of CD8-positive T lymphocytes in smokers with COPD. We examine whether airway inflammation alters with increasing severity of disease. ⋯ The precise roles of the CD8(+) T lymphocyte and the neutrophil in the pathogenesis of COPD still remain to be determined. Saetta M. Airway inflammation in chronic obstructive pulmonary disease.
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Am. J. Respir. Crit. Care Med. · Nov 1999
Pressure-release tracheal gas insufflation reduces airway pressures in lung-injured sheep maintaining eucapnia.
Although tracheal gas insufflation (TGI) has proved to be a useful adjunct to mechanical ventilation, end-inspiratory as well as end-expiratory pressures may increase. We investigated the ability of continuous-flow TGI to maintain eucapnia while reducing airway pressure (Paw) and tidal volume (VT). Seven sheep (36 +/- 2 kg) were ventilated using the Dräger Evita 4 in the pressure control plus mode where flow is released via the expiratory valve to maintain constant inspiratory pressure. ⋯ Tidal volume to dead space ratio (VD/VT) decreased preinjury from 0.49 +/- 0.1 to 0.18 +/- 0.2 and postinjury from 0.62 +/- 0.1 to 0.33 +/- 0.1 at a TGI flow of 10 L/min. The combination of the reverse flow TGI tube and a ventilator with an inspiratory pressure relief mechanism kept set end-inspiratory and end-expiratory pressures constant. This TGI system effectively reduced set Paw and VT while maintaining eucapnia.
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Am. J. Respir. Crit. Care Med. · Nov 1999
Acid-induced lung injury. Protective effect of anti-interleukin-8 pretreatment on alveolar epithelial barrier function in rabbits.
Although prior experimental work has demonstrated that anti-interleukin-8 (anti-IL-8) therapy reduces lung endothelial injury after acid instillation, there is no information regarding the effect of anti-IL-8 on the function of the alveolar epithelial barrier after acid-induced lung injury. Therefore, the primary objective of this study was to determine the effect of acid-induced lung injury on the function of the alveolar epithelium, and secondly to determine whether pretreatment with anti-IL-8 attenuates acid-induced injury to the lung epithelial barrier. Hydrochloric acid (pH = 1.5 in 1/3 normal saline) was instilled into the lungs of anesthetized, ventilated rabbits. ⋯ Pretreatment with anti-IL-8 antibody significantly reduced the acid-mediated increase in bi-directional transport of protein across the alveolar epithelium and restored alveolar fluid clearance to normal. The results indicate that acid instillation causes injury to the alveolar epithelial barrier that can be distinguished from the injury to the lung endothelium. Furthermore, pretreatment with anti-IL-8 therapy prevents acid-induced alveolar epithelial injury, a finding of potential clinical importance.