Experimental lung research
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Inhaled nitric oxide (iNO) improves gas exchange in about 60% of patients with acute respiratory distress syndrome (ARDS). Recruitment of atelectatic lung areas may improve responsiveness and preservation of spontaneous breathing (SB) may cause recruitment. Accordingly, preservation of SB may improve effectiveness of iNO. ⋯ Significant gas exchange improvements due to iNO were only achieved during unassisted SB with BIPAP (P <.05) but not during CMV or assisted SB. The authors conclude that effectiveness of iNO may be improved by unassisted SB during BIPAP but not by assisted SB. Thus combined iNO and unassisted SB is possibly most effective to improve gas exchange in severe hypoxemic ARDS.
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Comparative Study
High-frequency oscillation combined with arteriovenous extracorporeal lung assist reduces lung injury.
In order to optimize the lung-protective potential of high-frequency oscillatory ventilation (HFOV), it is currently recommended to maximize oscillatory frequencies. However, very high frequencies may lead to insufficient CO(2) elimination with severe respiratory acidosis. Arteriovenous extracorporeal lung assist (av-ECLA) allows near total CO(2) removal, thereby allowing for maximization of the lung-protective potential of HFOV. ⋯ The authors found that the combination of HFOV and av-ECLA (1) allows significant reductions in mean and peak airway pressures; and (2) reduces histological signs of lung inflammation in the basal regions of the lung. HFOV/av-ECLA reduces histological signs of lung inflammation compared to conventional lung-protective ventilation strategies. Thus, combination of HFOV and av-ECLA might be a further lung-protective tool if conventional ventilation strategies are failing.
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Intrinsic positive end-expiratory pressure (PEEP) occurs when airway outflow is higher than zero at end-expiration. Differences in the time constant among alveolar units may result in an uneven distribution of intrinsic PEEP. The authors conducted a computer simulation of a 2-compartment respiratory system and calculated intrinsic PEEP for each alveolar unit and confirmed it with a test-lung experiment. ⋯ A higher respiratory frequency and a larger percentage of inspiratory time resulted in an increase in the intrinsic PEEP at the central airway, as well as a wide difference in the intrinsic PEEP between airway units. These phenomena were confirmed by a 2-compartment test-lung study. The authors demonstrated and verified an uneven distribution of intrinsic PEEP in 2 different experiments, which raised a warning that some respiratory units might have much higher intrinsic PEEP than the intrinsic PEEP measured clinically.
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Neutrophilic inflammation is a key effector arm of the innate immune response. Neutrophils may contribute significantly to airway inflammation in certain asthma subtypes. The objective of this study is to investigate the innate immune responses of isolated airway and circulating neutrophils in asthma. ⋯ Resting and lipopolysaccharide (LPS)-stimulated circulating neutrophils had lower levels of TLR2 and IL-1beta gene expression in asthma, but were otherwise similar to healthy controls. No differences were seen for matrix metalloproteinase (MMP)-9 release in asthma. Innate immune responses of airway neutrophil cells are impaired in asthmatic subjects on prophylactic therapy and may impact on susceptibility to, and severity of, airway infections.
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The objective of this study was to determine if prolonged hyperoxia exposure would deplete antioxidants, resulting in excessive oxidative stress that would lead to oxidation of pulmonary surfactant and contribute to lung dysfunction. Rats were exposed to either hyperoxic (> 95% O(2)) or normoxic (21% O(2)) oxygen concentrations for 48 or 60 hours. Pulmonary compliance, inflammatory cells, and total protein levels were measured as indicators of lung injury. ⋯ Total surfactant and surfactant large aggregates were increased following 48 hours of hyperoxia exposure, with a further increase following 60 hours. Animals exposed to 60 hours of hyperoxia also demonstrated lower ascorbate levels in lung tissue, increased lipid peroxides in BAL, and increased oxidation of phosphatidylglycerol species in surfactant. This study demonstrates that the balance of oxidant/antioxidant components is disrupted within the lung during periods of hyperoxia, and that although surfactant lipids may be susceptible to oxidative damage, they do not likely represent a major mechanism for the lung dysfunction observed.