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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Sepsis remains the leading cause for noncardiac intensive care unit deaths in the United States. Despite recent advances in the treatment of this devastating condition, mortality and morbidity remain unacceptably high. Sepsis is characterized by a multitude of pathophysiological changes that include inflammation, metabolic derangements, hemodynamic alterations, and multiorgan dysfunction. ⋯ Recent data suggest that beta-blocker effects on metabolism, glucose homeostasis, cytokine expression, and myocardial function may be beneficial in the setting of sepsis. Although treating a potentially hypotensive condition with a drug with antihypertensive properties may initially seem counterintuitive, the metabolic and immunomodulatory properties of beta-blockers may be of benefit. It is the purpose of this review to discuss the effects of beta-blockers on the following: (1) metabolism, (2) glucose regulation, (3) the inflammatory response, (4) cardiac function, and (5) mortality in sepsis.
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To examine the effects of anticoagulants and the role of thrombin on neutrophil-platelet-endothelial cell interactions in septic shock. Controlled experiments using phase-contrast microscopy to study neutrophil, platelet, and endothelial cell interactions in flowing cell suspensions under simulated physiologic conditions. University research laboratory. ⋯ In addition, thrombin attenuated the effects of each of these agents on platelet-neutrophil aggregation, platelet activation, and neutrophil activation. These data suggest that H, A, ATIII, and rhAPC decrease sepsis-induced neutrophil-endothelial cell interactions. The reversal of this effect by thrombin suggests that these agents alter neutrophil-endothelial interactions through their anticoagulant effects and the resulting decrease in thrombin activity.