Journal of critical care
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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. ⋯ 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.
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Journal of critical care · Jun 1995
ReviewMolecular mechanisms of sepsis: molecular biology of the cell.
Complex and interrelated biological processes are at work in the expression of the host response to sepsis. To a large degree, these processes reflect drastic changes in the molecular workings of cells of the body. The protean nature of sepsis reflects this molecular adaptation. ⋯ It uses the process of endotoxin-induced cellular activation as its model and highlights important aspects of DNA promoter and enhancer processes in this activation. Specific examples of known promoter genes and genomic translation are described. This review serves as a "primer" for the subsequent three review articles in this series that will follow it in preceding issues.
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Journal of critical care · Mar 1995
ReviewPrevention of drug-induced nephrotoxicity in the intensive care unit.
Acute renal failure (ARF) occurs in 5% to 25% of all admissions to an intensive care unit (ICU). The development of ICU-associated ARF increases the average mortality from about 15% to more than 60%. ⋯ Recent studies suggest that a significant percent of hospital-acquired ARF is caused by nephrotoxins. This brief review will discuss the frequency of occurrence, pathophysiology, risk factors, clinical course, and prevention of nephrotoxicity that may occur after exposure to aminoglycosides, nonsteroidal anti-inflammatory drugs, and radiographic contrast agents.
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Journal of critical care · Dec 1994
ReviewEndothelial and vascular smooth muscle function in sepsis.
The vascular abnormalities that arise during sepsis imply disturbances in the delicately tuned homeostatic mechanisms of vascular endothelium and smooth muscle. In the microvasculature, smooth muscle tone represents a complex equilibrium among metabolic stimuli, hemodynamic forces, and neurohumoral influences. ⋯ In sepsis, derangement of normal autoregulation of perfusion, together with toxic effects of mediators, may be severe enough to result in organ dysfunction. Recent advances in vascular biology have illuminated a variety of targets, such as adhesion molecules, platelet activating factor, and inducible nitric oxide synthase for potential therapeutic intervention in sepsis.