Inflammatory response in microvascular endothelium in sepsis: role of oxidants.

Inflammatory response in microvascular endothelium in sepsis: role of oxidants.
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败血症微血管内皮的炎症反应:氧化剂的作用。

DOI:
10.3164/jcbn.2008026
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发表时间:
2008-05
影响因子:
2.4
通讯作者:
Wilson, John X.
Wilson, John X.
中科院分区:
医学4区
文献类型:
--
作者:
Cepinskas, Gediminas;Wilson, John X.

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脓毒症作为细菌感染引起的严重全身炎症反应,是临床上的一个主要问题。其特征在于在循环和受影响的器官中过量产生活性氧(ROS)。ROS的过度产生不可避免地导致微血管系统中的氧化应激,并且已经被认为是包括脓毒症在内的许多病理学中的致病事件。本文就氧化应激和亚硝化应激在脓毒症早期发病中的作用作一综述。微血管内皮细胞的变化,细胞类型,发生在所有器官,进行了讨论。脓毒症诱导氧化和亚硝化应激的机制,这些应激的功能后果,以及脓毒症微血管功能障碍的潜在辅助治疗被确定。
Sepsis, as a severe systemic inflammatory response to bacterial infection, represents a major clinical problem. It is characterized by the excessive production of reactive oxygen species (ROS) both in the circulation and in the affected organs. The excessive generation of ROS inevitably leads to oxidative stress in the microvasculature and has been implicated as a causative event in a number of pathologies including sepsis. In this review, we focus on the role of oxidative and nitrosative stress during the early onset of sepsis. Changes in microvascular endothelial cells, the cell type that occurs in all organs, are discussed. The mechanisms underlying septic induction of oxidative and nitrosative stresses, the functional consequences of these stresses, and potential adjunct therapies for microvascular dysfunction in sepsis are identified.
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