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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In septic shock (SS), dysfunction of many organ systems develops during the course of the illness, although the mechanisms are not clear. In earlier studies, we reported that lysozyme-c (Lzm-S), a protein that is released from leukocytes and macrophages, was a mediator of the myocardial depression and vasodilation that develop in a canine model of Pseudomonas aeruginosa SS. Whereas both of these effects of Lzm-S are dependent on its ability to intrinsically generate hydrogen peroxide, we subsequently showed that Lzm-S can also deposit within the vascular smooth muscle layer of the systemic arteries in this model. ⋯ In the in vivo model, Lzm-S accumulated in the kidney and the superior mesenteric artery. In a canine renal epithelial preparation, we further showed that Lzm-S can be taken up by the renal tubules to activate inflammatory pathways. We conclude that Lzm-S can deposit in the systemic vasculature and kidneys in SS, where this deposition could lead to acute organ dysfunction.
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Malnutrition is a risk factor for infection, compromising immune response. Glutamine (Gln) protects the lungs and distal organs in well-nourished septic and nonseptic conditions; however, no study to date has analyzed the effects of Gln in the presence of sepsis and malnutrition. In the present work, we tested the hypothesis that early therapy with intravenous Gln prevents lung and distal organ damage in septic malnourished rats. ⋯ In malnutrition-cecal ligation and puncture rats, Gln therapy yielded (a) reduced static lung elastance, alveolar collapse, inflammation (neutrophil infiltration, interleukin 6), and collagen deposition; (b) repair of types I and II epithelial cells; (c) no significant changes in heat shock protein 70 expression or heat shock factor 1 phosphorylation; (d) a greater number of M1 and M2 macrophages in lung tissue; and (e) less apoptosis in the lung, kidney, small intestine, and liver. In conclusion, early therapy with intravenous Gln reduced inflammation, fibrosis, and apoptosis, minimizing lung and distal organ injury, in septic malnourished rats. These beneficial effects may be associated with macrophage activation in the lung.
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Randomized Controlled Trial
Infusion of 7.2% NaCl/6% Hydroxyethyl Starch 200/0.5 in On-Pump Coronary Artery Bypass Surgery Patients: A Randomized, Single-Blind Pilot Study.
NaCl 7.2%/6% hydroxyethyl starch (HES) 200/0.5 (HSH) has shown its beneficial effects in cardiac surgery and immunomodulatory values in experiment and human studies. However, there is concern regarding detrimental renal effects of chloride and HES in the intensive care setting. ⋯ NaCl 7.2%/6% hydroxyethyl starch 200/0.5 does not lead to the increase in AKI incidence when used for the volume therapy in on-pump coronary artery bypass surgery patients. NaCl 7.2%/6% hydroxyethyl starch 200/0.5 usage enhanced neither tubular injury nor alteration of glomerular filtration. In addition, HSH can reduce the level of the inflammatory mediators after surgery.
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Clinical Trial Observational Study
Plasma Colloid Osmotic Pressure is an Early Indicator of Injury and Hemorrhagic Shock.
Hemorrhagic shock is the leading cause of traumatic deaths; many could be potentially prevented with appropriate resuscitation. However, to initiate resuscitation, one must identify patients with hemorrhagic shock early. In this article, we determined the associations between plasma colloid osmotic pressure (COP) and clinical outcomes in severely injured trauma patients. ⋯ Reduced plasma COP and serum protein in trauma patients are indicative of injury severity. In the absence of significant alterations in vital signs, plasma COP levels were associated with increased requirements for blood products and increased syndecan 1 shedding. We believe that plasma COP provides new insight in guiding resuscitation.
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Admission hypocoagulability has been associated with negative outcomes after trauma. The purpose of this study was to determine the impact of hypercoagulability after trauma on the need for blood product transfusion and mortality. ⋯ Approximately a quarter of trauma patients presented in a hypercoagulable state. Hypercoagulable patients required less blood products, in particular plasma. They also had a lower 24-h and 7-day mortality and lower rates of bleeding-related deaths. Further evaluation of the mechanism responsible for the hypercoagulable state and its implications on outcome is warranted.