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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Burn wound-related sepsis is associated with the development of systemic inflammatory response syndrome and multiple organ dysfunction syndrome (MODS). This study is aimed at investigating the development and progression of SIS and MODS in a mouse model of skin burn sepsis. C57BL/6J mice were randomly divided into the sham, burn, Pseudomonas, and burn/Pseudomonas groups. ⋯ The burn/Pseudomonas mice exhibited significantly higher levels of bacterial loads in different organs and serum endotoxin, interleukin 1β, interleukin 6, tumor necrosis factor α, and C-reactive protein than those in mice from the other groups (P < 0.05). The burn/Pseudomonas mice also displayed more severe liver, lung, and kidney tissue damage and impaired organ functions, particularly at 72 h after inoculation than did the burn and Pseudomonas groups of mice. Our data indicate that burn and P. aeruginosa infection induced severe sepsis and rapidly progressed into systemic inflammatory response syndrome and MODS in mice.
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We tested the effect of vagus nerve stimulation in endotoxin-induced intestinal tight junction injury in mice challenged with lipopolysaccharide (LPS) and examined the role of α7 nicotinic acetylcholine receptors (α7nAchR) in this process. Endotoxemia was induced by intraperitoneal injection of LPS (10 mg/kg) in male Balb/c mice. Samples were collected 12 h after LPS treatment. ⋯ Vagus nerve stimulation inhibited the upregulated activity of myosin light chain kinase and nuclear factor κB. In contrast, α-bungarotoxin (a specific α7nAchR antagonist, 0.1 μg/mouse) administered before vagus nerve stimulation significantly abolished these protective effects of vagus nerve stimulation. Our results for the first time confirmed that vagus nerve stimulation attenuated the disruption of tight junction in intestinal epithelium in endotoxemic mice, which was mediated through suppressing translocation of nuclear factor κB p65, downregulating myosin light chain kinase, and the α7nAchR may play an important role in this process.
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Although mitochondrial dysfunction is thought to contribute to the development of post-traumatic organ failure, current techniques to assess mitochondrial function in tissues are invasive and clinically impractical. We hypothesized that mitochondrial function in peripheral blood mononuclear cells (PBMCs) would reflect cellular respiration in other organs during hemorrhagic shock and resuscitation (HS&R). ⋯ All tissues including PBMC's demonstrated significant mitochondrial dysfunction following HS&R. Although PBMC and kidney mitochondrial function correlated well during hemorrhagic shock, the variability in mitochondrial response across tissues over the spectrum of hemorrhagic shock and resuscitation limits the usefulness of using PBMC's as a proxy for tissue-specific cellular respiration.