Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Alveolar type 2 (AT-2) cell apoptosis is an important mechanism during lung inflammation, lung injury, and regeneration. Blunt chest trauma has been shown to activate inflammatory cells such as alveolar macrophages (AMs) or neutrophils (polymorphonuclear granulocytes [PMNs]), resulting in an inflammatory response. The present study was performed to determine the capacity of different components/cells of the alveolar compartment (AMs, PMNs, or bronchoalveolar lavage [BAL] fluids) to induce apoptosis in AT-2 cells following blunt chest trauma. ⋯ In contrast, no apoptosis was induced in AT-2 cells incubated with supernatants of activated PMNs or BAL fluids of traumatized animals. In summary, blunt chest trauma induced apoptosis in AT-2 cells, possibly involving the extrinsic death receptor pathway. Furthermore, mediators released by AMs appeared to be involved in the induction of AT-2 cell apoptosis.
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Hemorrhagic shock (HS) is associated with the disruption of endothelial cell barrier leading to vascular hyperpermeability. Previous studies from our laboratory implicate reactive oxygen species (ROS) and the intrinsic apoptotic signaling cascades as mediators of vascular hyperpermeability after HS. Here we report the protective effects of alpha-lipoic acid, a natural antioxidant with antiapoptotic properties, against vascular hyperpermeability after HS. ⋯ Hemorrhagic shock resulted in vascular hyperpermeability and mitochondrial ROS formation. The activation of mitochondrial intrinsic apoptotic signaling pathway was evidenced from mitochondrial depolarization, an increase in cytochrome c release, and activation of caspase 3. alpha-Lipoic acid (100 mg/kg) given before the shock period attenuated vascular hyperpermeability, mitochondrial ROS formation, mitochondrial depolarization, cytochrome c release, and activation of caspase 3 (P < 0.05). Together, these results demonstrate that alpha-lipoic acid provides protection against vascular hyperpermeability by modulating the mitochondrial "intrinsic" apoptotic signaling.
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Meta Analysis
Frequency and predictors of ventilator-associated pneumonia recurrence: a meta-analysis.
Large clinical series focusing on the risk factors associated with recurrence after the onset of an initial episode of ventilator-associated pneumonia (VAP) produced inconsistent results. A meta-analysis would be helpful to shed light on the issue. Our objective was to estimate the frequency of VAP recurrence and to identify risk factors associated with it. ⋯ There was also evidence, albeit inconsistent, that severity of illness at intensive care unit admission was associated with VAP recurrence. Recurrence involves almost one in four cases of VAP and is associated with acute lung injury/acute respiratory distress syndrome and shock, but not with first-episode causative pathogens. Recognition of these predictors may permit the timely implementation of measures to prevent recurrence of VAP.