Oxidative stress and endothelial dysfunction during sepsis
Oxidative stress and endothelial dysfunction during sepsis
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DOI：
10.2741/3835
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发表时间：
2011-01-01
影响因子：
3.1
通讯作者：
Duranteau, Jacques
中科院分区：
文献类型：
--
作者：
Huet, Olivier;Dupic, Laurent;Duranteau, Jacques
内皮细胞活化和功能障碍在脓毒症的发病机制中起着关键作用。感染性休克时，内皮功能障碍涉及微循环障碍和器官功能障碍。活性氧（ROS）和活性氮（RNS）对内皮功能有几种潜在的重要作用，并与生理调节和疾病病理生理学有关。ROS的产生与其通过非酶和酶抗氧化剂系统的有效去除之间的不平衡可诱导内皮功能障碍，伴随血管张力的改变、细胞粘附特性（白细胞和血小板粘附）的增加、血管壁渗透性的增加和促凝状态。越来越多的证据支持脓毒症期间EC功能障碍的主要原因是细胞损伤的观点。ROS和RNS通过一系列机制导致线粒体功能障碍，并诱导坏死和凋亡性细胞死亡。了解内皮细胞中ROS和RNS产生的机制以及脓毒症中内皮功能障碍的原因可能有助于提供治疗策略来解决脓毒症中的内皮功能障碍和微循环衰竭。
Endothelial activation and dysfunction play a key role in the pathogenesis of sepsis. During septic shock, endothelial dysfunction is involved in microcirculation impairment and organ dysfunction. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have several potentially important effects on endothelial function and are implicated in physiological regulation and disease pathophysiology. The imbalance between the production of ROS and their effective removal by non-enzymatic and enzymatic antioxidants systems could induce endothelial dysfunction with alterations of vascular tone, increases in cell adhesion properties (leukocytes and platelet adhesion), increase in vascular wall permeability and a pro-coagulant state. Increasing evidence supports the idea that the principal cause of EC dysfunction during sepsis is cell injury. ROS and RNS contribute to mitochondrial dysfunction by a range of mechanisms and induce both necrotic and apoptotic cell death. Understanding the mechanisms underlying the generation of ROS and RNS in endothelial cells and the causes of endothelial dysfunction in sepsis may help provide therapeutic strategies to tackle endothelial dysfunction and microcirculatory failure in sepsis.