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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There are very few data regarding the effects of norepinephrine uptitration on global and regional hemodynamics in cardiogenic shock. We studied 25 patients with shock secondary to myocardial infarction successfully treated with percutaneous coronary intervention. Before the inclusion, 16 of 25 patients presented a cardiac arrest in the presence of medical staff. ⋯ The StO2 recovery slope and delta StO2, respectively, increased from 3.0% ± 1.3%/s to 3.6% ± 1.3%/s and 10% ± 3% to 14% ± 4%, whereas StO2 did not change (83% ± 6% to 83% ± 7%). After H1, norepinephrine was decreased to basal values, and all variables returned to baseline. In conclusion, a short-term increase in MAP with norepinephrine in resuscitated cardiogenic shock complicated by postreperfusion disease is associated with better cardiac performance and improved microcirculatory variables.
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Sepsis-induced inflammation in the gut/peritoneal compartment occurs early in sepsis and can lead to acute lung injury (ALI). We have suggested that inflammatory ascites drives the pathogenesis of ALI and that removal of ascites with an abdominal wound vacuum prevents ALI. We hypothesized that the time- and compartment-dependent changes in inflammation that determine this process can be discerned using principal component analysis (PCA) and Dynamic Bayesian Network (DBN) inference. ⋯ These combined in vivo and in silico studies suggest that in this clinically realistic paradigm of sepsis, endotoxin drives the inflammatory response in the ascites, interplaying with lung dysfunction in a feed-forward loop that exacerbates inflammation and leads to endothelial dysfunction, systemic spillover, and ALI; PST partially modifies this process.
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Inflammatory responses can induce microvascular and endothelial dysfunction, which is associated with the development of sepsis. This study is aimed at examining the concentrations of plasma tissue factor (TF), von Willebrand factor (vWF), and tumor necrosis factor-α (TNF-α) in patients with sepsis and at determining how septic plasma (SP) regulates TF and vWF expression and p38 mitogen activated protein kinase (p38 MAPK)/nuclear factor-κB (NF-κB) pathways in human endothelial cells. The concentrations of plasma TF, vWF, and TNF-α in 22 septic patients and eight healthy controls (HCs) were examined by enzyme-linked immunosorbent assay, and their potential association with disease severity was analyzed. ⋯ Furthermore, treatment with SP, but not NP, induced TF and vWF production in HUVECs in a dose- and time-dependent manner, which was associated with sequential activation of the p38 MAPK and NF-κB pathways. Septic plasma induced HUVEC apoptosis, which was inhibited by activating the NF-κB pathway. The sepsis-related inflammatory factors promoted endothelial cell activation, dysfunction, and apoptosis through activation of the p38 MAPK pathway that was regulated by NF-κB signaling.
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The objective of this study was to investigate the effects of pyruvate-containing fluids on peritoneal resuscitation (PR), following intravenous fluid resuscitation from hemorrhagic shock (HS) in rats. ⋯ Peritoneal resuscitation with hyperosmolar fluids attenuated visceral vasoconstriction and splanchnic hypoperfusion and improved the intestinal barrier protein and organ function following conventional fluid resuscitation from severe HS in rats. Pyruvate was superior to lactate in PDS as PR fluids, and 2.2% pyruvate was the optimal fluid in PR.
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Mechanical ventilation can cause structural and functional disturbances in the lung termed ventilator-induced lung injury (VILI). The aim of this study was to evaluate whether BML-111, a lipoxin receptor agonist, could attenuate VILI. Following induction of anesthesia and tracheostomy, Sprague-Dawley rats were ventilated with low tidal volume (6 mL/kg) or high tidal volume (20 mL/kg, HVT) for 4 h. ⋯ Administration with BML-111 suppressed the decrement of the nuclear factor κB (NF-κB) inhibitor IκB-α, diminished NF-κB activation, and reduced activation of mitogen-activated protein kinase in VILI. This study indicates that BML-111 attenuated VILI via a NF-κB and mitogen-activated protein kinase dependent mechanism. BML-111 may be a promising strategy for alleviation of VILI in patients subjected to mechanical ventilation.