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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Elucidation of early metabolic signatures that predict survival in septic shock might help clinicians in prioritizing individual patient treatment. In this preliminary investigation, we examined plasma metabolome and clinical features in a subset of 20 patients with septic shock, enrolled in the multicenter Albumin Italian Outcome Sepsis (ALBIOS, NCT00707122). ⋯ Our preliminary results suggest that increased KYN, that may contribute to hypotension in sepsis, as well as alterations of different LPC and PC species, able to modulate immune and inflammatory responses, might represent not only a risk factor for septic shock patients but important pathophysiologic mechanisms deserving further investigation.
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Co-morbidities are a confounding factor increasing intensive care mortality. Atherosclerosis and chronic kidney disease (CKD) not only influence renal function, e.g. reduce glomerular filtration rate (GFR), but may also cause endothelial barrier dysfunction (BD). Fluid extravasation due to BD is a risk factor in circulatory shock. In murine CKD models, ambivalent data are reported on regulating mechanisms of BD. Therefore, we investigated the role of BD in swine with reduced GFR, atherosclerosis and impaired tissue receptor protein expression (EPO-R, PPAR-β). ⋯ Supported by the DFG (SFB 1149).
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Sepsis leads to an enhanced susceptibility to secondary infections due to development of immunosuppression. We have previously shown that dysfunctional dendritic cells (DCs) that characteristically secrete IL 10 differentiate from bone marrow (BM) during polymicrobial sepsis and contribute to immunosuppression. ⋯ So far, unidentified cells in the peritoneal cavity are challenged in a CXCR4-dependent manner after CLP and indirectly induce the migration of CD4 + DCs from blood into the BM where they favor the differentiation of dysfunctional DCs.
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Dysfunction of the intestinal barrier plays an important role in the pathological process of heatstroke. Omega-3 (or n-3) polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), help protect the intestinal mucosal barrier. This study assessed if pretreating rats with EPA or DHA could alleviate heat stress-induced damage to the intestinal barrier caused by experimental heatstroke. ⋯ Our results indicate that EPA pretreatment is more effective than DHA pretreatment in attenuating heat-induced intestinal dysfunction and preventing TJ damage. Enhanced expression of TJ proteins that support the epithelial barrier integrity may be important for maintaining a functional intestinal barrier during heatstroke.
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Nitric oxide was suggested to regulate p53-dependent expression of heat shock proteins and changes in cellular metabolism. ⋯ Supported by EU(ESF) and NSRF-THALES.