Critical care medicine
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Aging is associated with increased inflammation following sepsis. The purpose of this study was to determine whether this represents a fundamental age-based difference in the host response or is secondary to the increased mortality seen in aged hosts. ⋯ Aged mice are more likely to die of sepsis than young mice when subjected to an equivalent insult, and this is associated with increases in both systemic and local inflammation. There is an exaggerated local but not systemic inflammatory response in aged mice compared with young mice when mortality is similar. This suggests that systemic processes that culminate in death may be age independent, but the local inflammatory response may be greater with aging.
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Critical care medicine · Mar 2009
Gene-expression profiling of peripheral blood mononuclear cells in sepsis.
It has been shown that gene-expression profiling of circulating neutrophils could identify signature genes of sepsis. However, whether similar transcriptional changes occurred in peripheral blood mononuclear cells (PBMC) was not known. Using microarray technology, we performed gene-expression profiling of PBMC to identify signature genes that distinguish sepsis from noninfectious causes of systemic inflammatory response syndrome (SIRS), between Gram-positive and Gram-negative sepsis. ⋯ There was evidence of sepsis-related immunosuppression and reduced inflammatory response in mononuclear cells on a transcriptome level. These characteristic transcriptional changes can be used to aid the diagnosis of sepsis.
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Critical care medicine · Mar 2009
Pulmonary lesion induced by low and high positive end-expiratory pressure levels during protective ventilation in experimental acute lung injury.
To investigate the effects of low and high levels of positive end-expiratory pressure (PEEP), without recruitment maneuvers, during lung protective ventilation in an experimental model of acute lung injury (ALI). ⋯ In the present nonrecruited ALI model, protective mechanical ventilation with lower and higher PEEP levels than required for better oxygenation increased Est, L and DeltaP2, L, the amount of atelectasis, and PCIII mRNA expression. PEEP selection titrated for a minimum elastance and maximum oxygenation may prevent lung injury while deviation from these settings may be harmful.
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Critical care medicine · Mar 2009
Inflammatory and circulatory effects of the reduction of endotoxin concentration in established porcine endotoxemic shock--a model of endotoxin elimination.
To study whether a reduction of the endotoxin load, once a generalized inflammatory state has been established, reduces the inflammatory response and endotoxin-induced effects on circulation, hypoperfusion, and organ dysfunction. ⋯ Termination of the endotoxin infusion represents an incontestable model of endotoxin concentration reduction. Endotoxin elimination strategies applied at the TNF-alpha peak or later will have very little or no effect on TNF-alpha-mediated toxicity. Nevertheless, there was an effect on the leukocyte response that was associated with an improvement in respiratory function and microcirculation, making it impossible to rule out fully the beneficial effect of this strategy. However, the effects were limited in relation to the magnitude of the endotoxin concentration reduction and the very early application of the antiendotoxin measure.
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Critical care medicine · Mar 2009
Pulmonary atelectasis during low stretch ventilation: "open lung" versus "lung rest" strategy.
Limiting tidal volume (VT) may minimize ventilator-induced lung injury (VILI). However, atelectasis induced by low VT ventilation may cause ultrastructural evidence of cell disruption. Apoptosis seems to be involved as protective mechanisms from VILI through the involvement of mitogen-activated protein kinases (MAPKs). We examined the hypothesis that atelectasis may influence the response to protective ventilation through MAPKs. ⋯ Low stretch strategies provide similar attenuation of VILI. However, low stretch/lung rest strategy is associated to less apoptosis and more ultrastructural evidence of cell damage possibly through MAPKs-mediated pathway.