Endothelial activation, dysfunction and permeability during severe infections
Endothelial activation, dysfunction and permeability during severe infections
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DOI：
10.1097/moh.0b013e328345a3d1
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发表时间：
2011-05-01
影响因子：
3.2
通讯作者：
Liles, W. Conrad
中科院分区：
文献类型：
--
作者：
Lee, Warren L.;Liles, W. Conrad
综述的目的在过去的几年里，我们对微血管内皮在严重全身性感染发病机制中的作用的认识有了重大进展，最近的发现内皮细胞活化和功能障碍直接导致败血症和其他严重全身性感染的发病率和死亡率。弥漫性内皮激活和功能障碍的最终结果可能是微血管屏障完整性的丧失，导致组织水肿、休克和多器官衰竭。内皮细胞活化也导致血管生成素-2增加，这是已知的不稳定屏障功能和促进inflammation.SummaryThe分泌的内皮生长因子，血管生成素-2和血管生成素-1的比例似乎是一个有用的预后工具，在严重感染。最后，增强内皮屏障完整性的药物可能被证明可用作脓毒症的治疗方法。
Purpose of reviewOver the last few years, there have been major advances in our understanding of the role of the microvascular endothelium in the pathogenesis of severe, systemic infections.Recent findingsEndothelial activation and dysfunction contribute directly to the morbidity and mortality of sepsis and other, severe systemic infections. The end-result of diffuse endothelial activation and dysfunction may be the loss of microvascular barrier integrity, leading to tissue edema, shock and multiple organ failure. Endothelial activation also leads to an increase in angiopoietin-2, which is known to destabilize barrier function and promote inflammation.SummaryThe ratio of the secreted endothelial growth factors, angiopoietin-2 and angiopoietin-1 appears to be a useful prognostic tool during severe infections. Finally, agents that enhance endothelial barrier integrity may prove useful as therapies for sepsis.