Taylor D E, Piantadosi C A
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Crit Care. 1995 Sep;10(3):122-35. doi: 10.1016/0883-9441(95)90003-9.
The high mortality associated with sepsis syndrome and multiple organ dysfunction syndrome has persisted despite extraordinary research efforts in the laboratory and the intensive care unit. These syndromes produce systemic tissue damage that is likely to result from widespread inflammation and subsequent endothelial injury. This article reviews the oxidative metabolic effects and responses to sepsis syndrome at several levels: the oxygen transport system, the cell, and the mitochondrion. Specifically, aerobic metabolism of carbon substrates and oxygen is altered in sepsis. As a result of systemic inflammation and nonmetabolic oxygen use, oxidative stress may occur both outside and inside the cell. The consequences of these oxidative processes during sepsis may be ongoing cell damage mediated by reactive oxygen and nitrogen oxide species that culminates in multisystem organ failure.
尽管在实验室和重症监护病房进行了大量研究，但脓毒症综合征和多器官功能障碍综合征相关的高死亡率一直存在。这些综合征会导致全身性组织损伤，这可能是由广泛的炎症和随后的内皮损伤引起的。本文从几个层面综述了脓毒症综合征的氧化代谢效应及反应：氧运输系统、细胞和线粒体。具体而言，脓毒症时碳底物和氧的有氧代谢会发生改变。由于全身性炎症和非代谢性氧利用，细胞内外都可能发生氧化应激。脓毒症期间这些氧化过程的后果可能是由活性氧和氮氧化物介导的持续细胞损伤，最终导致多系统器官衰竭。
