tailieunhanh - Báo cáo y học: "bench-to-bedside review: Endothelial cell dysfunction in severe sepsis: a role in organ dysfunction"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về y học đề tài: Bench-to-bedside review: Endothelial cell dysfunction in severe sepsis: a role in organ dysfunction? | Critical Care April 2003 Vol 7 No 2 Vallet Review Bench-to-bedside review Endothelial cell dysfunction in severe sepsis a role in organ dysfunction Benoit Vallet Professor Department of Anesthesiology and Intensive Care and Department of Pharmacology University Hospital Lille France Correspondence Benoit Vallet bvallet@ Published online 6 January 2003 Critical Care 2003 7 130-138 DOI cc1864 This article is online at http content 7 2 130 2003 BioMed Central Ltd Print ISSN 1364-8535 Online ISSN 1466-609X Abstract During the past decade a unifying hypothesis has been developed to explain the vascular changes that occur in septic shock on the basis of the effect of inflammatory mediators on the vascular endothelium. The vascular endothelium plays a central role in the control of microvascular flow and it has been proposed that widespread vascular endothelial activation dysfunction and eventually injury occurs in septic shock ultimately resulting in multiorgan failure. This has been characterized in various models of experimental septic shock. Now direct and indirect evidence for endothelial cell alteration in humans during septic shock is emerging. The present review details recently published literature on this rapidly evolving topic. Keywords coagulation endothelial cell monocyte sepsis shock tissue factor tissue oxygenation tissue perfusion vascular reactivity The vascular endothelium regulates the flow of nutrient substances diverse biologically active molecules and the blood cells themselves. This role of endothelium is achieved through the presence of membrane-bound receptors for numerous molecules including proteins lipid transporting particles metabolites and hormones as well as through specific junction proteins and receptors that govern cell-cell and cell-matrix interactions 1 2 . Endothelial dysfunction and or injury with subendothelium exposure facilitates leucocyte and platelet aggregation and aggravation of coagulopathy. .