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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Comparative Study
Altered hemodynamic counter-regulation to hemorrhage by acute moderate alcohol intoxication.
The incidence of traumatic injury, frequently associated with hemorrhagic shock, is higher in the alcohol-intoxicated individual. The outcome, as it pertains to both morbidity and mortality of this population, is partly dependent on duration of alcohol exposure and levels of blood alcohol at time of injury. In previous studies, we demonstrated that prolonged alcohol intoxication (15-h duration) produces marked hemodynamic instability and exacerbated early lung proinflammatory cytokine expression after hemorrhagic shock. ⋯ Only the hemorrhage-induced rise in lung IL-6 and tumor necrosis factor alpha was prevented by alcohol administration. In contrast, spleen cytokine responses to hemorrhage were not altered by alcohol administration. These results indicate that moderate acute alcohol intoxication results in significant modulation of hemodynamic and neuroendocrine responses to hemorrhagic shock.
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Mechanical ventilation (MV) with large tidal volumes (V(T)) causes ventilator induced lung injury. Whereas immediate effects of short-term injurious ventilation are well studied, little is known about its long-term effects. We aimed to establish an animal model of selective injurious MV, permitting assessment of the long-term course of ventilation-induced lung injury. ⋯ Twenty-four hours after MV, alveolar levels of humoral (tumor necrosis factor alpha, interleukin 6) and cellular (polymorphonuclear leukocytes) inflammatory markers were increased, and histological alterations were present in lungs ventilated with high V(T). A delayed decrease in PaO2 was noted 24 h after MV, with high V(T) delivered to one lung as compared with low V(T) delivered to both lungs. This animal model permits assessment of the long-term course of ventilation-induced lung injury and shows that pulmonary inflammation and histological alterations are present 24 h after unilateral injurious ventilation.
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Shock states are characterized by a pronounced activation of numerous cell types that lead to an acute inflammatory reaction. The exact mechanism by which these inflammatory cells are activated is not known. Numerous studies have implicated the gastrointestinal tract as one of the main sites for the generation of inflammatory mediators and initiation of an acute systemic response. ⋯ Studies that included information concerning the role of pancreatic enzymes in shock were then summarized. Our article serves to review the current hypotheses on how digestive enzymes produced by the pancreas may play a pivotal role in initiating the systemic inflammatory response. We further hypothesize how these enzymes and/or their products may ultimately contribute to multiorgan failure and death.
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A severe burn leads to hypermetabolism and catabolism resulting in compromised function and structure of essential organs. The massive release of cytokines is implicated in this hypermetabolic response. The aim of the present study was to compare cytokine expression profiles from severely burned children without signs of infections or inhalation injury (n = 19) to the cytokine profiles from normal, noninfected, nonburned children (n = 14). ⋯ After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis. The cytokine concentrations decrease during 5 weeks after burn but remain elevated over nonburned values. Furthermore, the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.
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Comparative Study
Prognostic value of interleukin 6, procalcitonin, and C-reactive protein levels in intensive care unit patients during first increase of fever.
To investigate the prognostic value of interleukin 6 (IL-6), procalcitonin (PCT), and C-reactive protein (CRP) in critically ill patients during the first increase of fever, serum levels were measured in 38 patients admitted to intensive care unit of the Department of Medicine, Klinikum Grosshadern, University of Munich, immediately after increase of body temperature more than 38.3 degrees C. Ten healthy controls were also included for comparison. The onset of fever was accompanied by elevated circulating levels of all the 3 markers in comparison with healthy controls. ⋯ Sensitivity, specificity, positive, and negative predictive values calculated from median levels was higher for IL-6 compared with PCT and CRP. Areas under receiver characteristic operating curves revealed the highest area under the curve for IL-6 in contrast to PCT and CRP. These data suggest that IL-6 rather than PCT or CRP may be an early predictor of mortality in patients with onset of fever and identify patients, who need intensive monitoring to initiate appropriate therapy at an early stage.