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• W1997208002 endingPage "135" @default.
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• W1997208002 abstract "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." @default.
• W1997208002 created "2016-06-24" @default.
• W1997208002 creator A5055502434 @default.
• W1997208002 creator A5070009351 @default.
• W1997208002 date "1995-09-01" @default.
• W1997208002 modified "2023-10-16" @default.
• W1997208002 title "Oxidative metabolism in sepsis and sepsis syndrome" @default.
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• W1997208002 doi "https://doi.org/10.1016/0883-9441(95)90003-9" @default.
• W1997208002 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7496449" @default.
• W1997208002 hasPublicationYear "1995" @default.
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