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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Lymphatic reactivity has been shown to exhibit a biphasic change following hemorrhagic shock, and nitric oxide (NO) is involved in this process. However, the precise mechanism responsible for NO regulation of the lymphatic reactivity along with the progression of hemorrhagic shock is unclear. Therefore, the present study was to investigate how NO participates in regulating the shock-induced biphasic changes in lymphatic reactivity and its underlying mechanisms. ⋯ Meanwhile, NOS antagonist (L-NAME), protein kinase G (PKG) inhibitor (KT-5823), and soluble guanylate cyclase inhibitor (ODQ) increased the reactivity of shock 2 h-lymphatics, whereas KATP opener (pinacidil) inhibited these elevated effects induced by either L-NAME, ODQ, or KT-5823. Taken together, these results indicate that NO regulation of lymphatic reactivity during shock involves both cAMP-PKA-KATP and cGMP-PKG-KATP pathways. These findings have potential significance for the treatment of hemorrhagic shock through regulating lymphatic reactivity.
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Our goal is to determine the prognostic value of serum N-terminal prohormone of brain natriuretic peptide (NT-proBNP), leukocytosis, and hyperglycemia in patients with severe hand, foot, and mouth disease (HFMD). ⋯ Routine admission surveillance for NT-proBNP is useful for identifying patients with HFMD at risk for mortality. Further studies are needed to determine whether early intervention in patients with highly elevated NT-proBNP can improve outcome.
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Translating murine data to the human situation, we proposed that the level of peroxisome proliferator-activated receptor γ (PPARγ) expression in T cells from septic patients correlates with clinical outcome. In this preliminary report, we analyzed PPARγ mRNA expression in CD3 T cells derived from blood of a very small number of septic patients (n = 18) on various days up to 2 weeks after the initial diagnosis. CD3 T cell count was determined by flow cytometry. ⋯ Setting two arbitrary limits: patients with a PPARγ expression in T cells higher than 7,000 copies/25 ng mRNA, of whom five of six patients died during the ICU stay, and patients with a T cell count below 100 T cells/μL blood, of whom five of eight patients died, we identified a correlation between sepsis survival and low T cell number, paired with high T cell-specific PPARγ expression. Among all 18 sepsis patients, four fulfilled the criteria for both arbitrary settings and all four of these patients subsequently died. We suggest that both high PPARγ expression in T cells and low absolute T cell number in blood of septic patients may have the potential as a new prognostic marker for a poor sepsis outcome.
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To determine which strategy of early post-cardiac arrest hemodynamic resuscitation was associated with best clinical outcomes. We hypothesized that higher mean arterial pressure (MAP) achieved using IV fluids over vasopressors would yield better outcomes. ⋯ Early post-return of spontaneous circulation hemodynamic resuscitation achieving higher MAP using fluid preferentially over vasopressors is associated with improved survival to hospital discharge as well as better lactate clearance.
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The mechanisms involved in septic anorexia are mainly related to the secretion of inflammatory cytokines. The term endozepines designates a family of neuropeptides, including the octadecaneuropeptide (ODN), originally isolated as endogenous ligands of benzodiazepine receptors. Previous data showed that ODN, produced and released by astrocytes, is a potent anorexigenic peptide. We have studied the effect of sepsis by means of a model of cecal ligation and puncture (CLP) on the hypothalamic expression of endozepines (DBI mRNA and protein levels), as well as on the level of neuropeptides controlling energy homeostasis mRNAs: pro-opiomelanocortin, neuropeptide Y, and corticotropin-releasing hormone. In addition, we have investigated the effects of two inflammatory cytokines, TNF-α and IL-1β, on DBI mRNA levels in cultured rat astrocytes. ⋯ These results suggest that during sepsis, hypothalamic mRNA encoding endozepines, anorexigenic peptide as well as stress hormone could play a role in the anorexia/cachexia associated with inflammation due to sepsis and we suggest that this hypothalamic mRNA expression could involve TNF-α.