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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Lymphocyte exhaustion was recently recognized as a mechanism of immunosuppression in sepsis. While B cells are known to play pivotal roles in bacterial infection and sepsis, changes in B-cell-mediated humoral immunity have not been evaluated in critically ill septic patients. We aimed to investigate changes in humoral immunity caused by defective B-cell function during severe sepsis. ⋯ This finding was clinically relevant, as elderly patients with decreased IgM production might be more susceptible to infection by Gram-negative bacteria and fungi. Reduced immunocompetent B cells may be related to increased secondary infection after sepsis, especially in the elderly. Finally, impaired humoral immunity with increased CD21 exhausted B cells and insufficient immunoglobulin M production may be a critical immunological change in sepsis.
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Trauma-Related Acute Lung Injury Develops Rapidly Irrespective of Resuscitation Strategy in the Rat.
Acute lung injury (ALI) has been observed clinically after severe trauma. We have recently developed a rat model of polytrauma that shows evidence of multi-organ failure and coagulopathy. In this study, we investigate whether ALI occurs after severe trauma and resuscitation, and the cellular mechanisms involved. ⋯ This study shows that trauma related acute lung injury occurs early after polytrauma and hemorrhage in rat. This ALI is secondary to the trauma, and likely due to an elevation in leukocytes, platelets, inflammatory cytokines and myeloperoxidase in the lung tissue prior to any resuscitation. Resuscitation with either LR or whole blood demonstrated similar lung edema. Blood was neither more protective nor more damaging than LR during early resuscitation.
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Hemorrhage is the leading cause of preventable death in trauma, and hemorrhage from noncompressible junctional anatomic sites is particularly difficult to control. The current standard is QuikClot Combat Gauze packing, which requires 3 min of compression. We have created a novel dressing with calcium carbonate microparticles that can disperse and self-propel upstream against flowing blood. ⋯ PTG animals maintained lower serum lactate and higher hemoglobin concentrations than NPTG (P <0.05) suggesting PTG decreased severity of subsequent hemorrhagic shock. However, total blood loss, Lactated Ringer infusion volumes, and mean arterial pressures of surviving animals were not different between groups (P >0.05). Thus, in this swine model of junctional arterial hemorrhage, gauze with self-propelled, prothrombotic microparticles improved survival and 2 indicators of hemorrhagic shock when applied without compression, suggesting this capability may enable better treatment of non-compressible junctional wounds.
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Despite being the leading cause of death in the United States for individuals 46 years and younger and the primary cause of death among military service members, trauma care research has been underfunded for the last 50 years. Sustained federal funding for a coordinated national trauma clinical research program is required to advance the science of caring for the injured. The Department of Defense is committed to funding studies with military relevance; therefore, it cannot fund pediatric or geriatric trauma clinical trials. ⋯ CNTR's member organizations are the American Association for the Surgery of Trauma (AAST), the American College of Surgeons Committee on Trauma (ACS COT), the Eastern Association for the Surgery of Trauma (EAST), the Western Trauma Association (WTA), and the National Trauma Institute (NTI). CNTR advocates for sustained federal funding for a multidisciplinary national trauma research program to be conducted through a large clinical trials network and a national trauma research repository. The initial advocacy and research activities underway to accomplish these goals are presented.
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Severe burn results in systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction (MOD). Currently, large-animal models of burn-induced SIRS/MOD mostly use secondary insults resulting in a paucity of knowledge on the effect of burn alone on different organ systems. The objective of the current study was to develop and characterize a large animal model of burn-induced SIRS over the course of 2 weeks. ⋯ Intestinal structure as well as enterocyte homeostasis was also disrupted. All of these organ abnormalities recovered to varying degrees by 14 days post-burn. We report a unique reproducible large animal model of burn-induced SIRS that can be tailored to specific organ systems for investigation into potential immunomodulatory interventions that prevent organ failure or promote organ recovery after burn injury.