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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Complement system activation is recognized as a deleterious component of the mammalian physiological response to traumatic injury with severe hemorrhage (TH). Female Yorkshire swine were subjected to a simulated austere prehospital battlefield scenario. Each animal underwent controlled hemorrhage of 22 mL/kg at 100 mL/min rate for approximately 10 min followed by soft tissue injury, femur fracture, and spleen injury. ⋯ Immunohistochemical analyses revealed that C1INH administration following TH markedly reduced complement activation and deposition in tissues. Importantly, C1INH administration prolonged survival of animals particularly in those which received resuscitation fluid infusion. Our data urge early administration of C1INH to limit organ damage and prolong survival of those injured in the battlefield.
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In response to infectious and, in some instances, noninfectious insults, the affected tissues/cells of the host undergo inflammation. However, uncontrolled inflammation could be detrimental to the host, resulting in inflammatory disease, such as inflammatory lung disease. Although the etiology of the disease is well defined, the underling pathogenesis is still incompletely understood. ⋯ Nevertheless, the mechanism through which ACE2 plays a role in inflammatory lung disease has not been clearly identified. In an attempt to summarize current literature findings and progress made in uncovering the role of ACE2 in inflammatory lung disease, this review will focus on recent studies examining pulmonary ACE2 biology, its roles in inflammatory lung disease pathogenesis and possible underlying mechanisms. Finally, we will discuss pulmonary ACE2 as a potential therapeutic target for inflammatory lung disease.
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Previous studies have suggested that lowering heart rate (HR) by selective β1-blockers improves sepsis-induced cardiac and vascular dysfunction primarily by decreasing proinflammatory pathways. However, the impact of isolated heart rate reduction (HRR) on hemodynamics and inflammatory pathways remains unknown. The present study was designed to assess the effects of HRR by ivabradine, an If channel inhibitor, on cardiovascular function and inflammatory pathways in peritonitis-induced septic shock in rats. ⋯ Isolated HRR by ivabradine in an experimental model of septic shock does not appear to be associated with any effect on the tested parameters of cardiac function or on vascular responsiveness to vasopressors. Moreover, in this setting, ivabradine does not alter the circulating levels of selected pro/anti-inflammatory cytokines or cardiac and vascular NF-κB/IκBα protein expression levels.
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Hypertonic crystalloid solutions, colloids, and fresh whole blood (FWB) have all been proposed for prehospital resuscitation after hemorrhage. However, there are no direct comparisons of the efficacy of these different fluids. We compared Hextend, 3% hypertonic saline (HS), and FWB in a porcine model of hemorrhagic shock. ⋯ HS performed inferiorly to Hextend as a volume expanding resuscitative fluid after hemorrhage. On the basis of our data, we would recommend the use of Hextend over 3% saline in far forward resuscitation after hemorrhage.