Critical care : the official journal of the Critical Care Forum
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Muscle weakness is highly prevalent during acute critical illness, with the poor exercise performance that occurs after critical illness being recognized as a consequence of skeletal muscles weakness. Advanced techniques to measure peripheral muscle strength are available, but they have limited use in the clinical setting. ⋯ At present, the mechanisms that underlie skeletal muscle wasting and weakness are poorly understood, but use of rehabilitation early in critical illness appears to have beneficial effects on outcome. The future direction will be to determine the underlying mechanisms as well as developing rehabilitation programmes during both the acute and the post critical illness stages.
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Results from clinical studies have provided evidence for the importance of leukocyte-endothelial interactions in the pathogenesis of pulmonary diseases such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), as well as in systemic events like sepsis and multiple organ failure (MOF). The present study was designed to investigate whether alveolar stretch due to mechanical ventilation (MV) may evoke endothelial activation and inflammation in healthy mice, not only in the lung but also in organs distal to the lung. ⋯ Our data implicate that MV causes endothelial activation and inflammation in mice without pre-existing pulmonary injury, both in the lung and distal organs.
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Dehydroepiandrosterone (DHEA) improves survival after trauma and sepsis, while mechanisms of action are not yet fully understood. Therefore, we investigated the influence of DHEA on local cytokine expression in a two-hit model. ⋯ The improved outcome after DHEA treatment and trauma is coherent with restoration of TNF-alpha in liver and lung after 48 hours and a counter-regulatory attenuation of TNF-alpha in liver after 96 hours. Thus, DHEA seems to act, time and organ dependent, as a potent modulator of TNF-alpha expression.