Interleukin-1-mediated acute lung injury and tolerance to oxidative injury.

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Interleukin-1-mediated acute lung injury and tolerance to oxidative injury.

Interleukin-1 (IL-1) is a highly potent molecule that has a myriad of effects in biologic systems. This brief review describes some of our findings on the effects of IL-1 in biologic systems. On the one hand, IL-1 treatment caused a neutrophil-dependent acute edematous lung injury that resembled changes in the lungs of patients with the acute respiratory distress syndrome (ARDS). On the other h...

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Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats

Objective(s):Therapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury, the exact mechanisms are still less known in the hyperoxic acute lung injury (HALI).   Materials ...

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Oxidative stress: acute and progressive lung injury.

Oxidative stress in lung often occurs in humans during acute lung injury (ALI) and in the acute respiratory distress syndrome. The lung inflammatory response may proceed to the development of pulmonary fibrosis, a devastating complication that occurs in premature infants after prolonged exposure to high oxygen concentrations. Oxidant-related ALI can be induced by airway deposition of lipopolysa...

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Oxidative stress and acute lung injury.

Acute lung injury (ALI) and its most severe form, the acute respiratory distress syndrome (ARDS) are frequent complications in critically ill patients and are responsible for significant morbidity and mortality (1, 2). Treatment of the underlying disease and excellent supportive care using “lung-protective” strategies of mechanical ventilation (3) contribute to successful clinical outcomes. How...

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ژورنال

عنوان ژورنال: Environmental Health Perspectives

سال: 1994

ISSN: 0091-6765,1552-9924

DOI: 10.1289/ehp.94102s1075