Critical Care Medicine

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Critical Care Medicine:
doi: 10.1097/CCM.0b013e3182120cb8
Laboratory Investigations

Ascorbic acid attenuates lipopolysaccharide-induced acute lung injury*

Fisher, Bernard J. MS; Seropian, Ignacio M. MD, PhD; Kraskauskas, Donatas DVM; Thakkar, Jay N. PhD; Voelkel, Norbert F. MD; Fowler, Alpha A. III MD; Natarajan, Ramesh PhD

Supplemental Author Material


In the article on page 1454 of the June issue, an incorrect Figure 6A was used. The corrected figure is below:

Critical Care Medicine. 39(8):2022, August 2011.

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Objective: Sepsis-induced lung injury is a persisting clinical problem with no direct therapy. Recent work suggests that intravenously infused ascorbic acid improves the circulatory dysfunction of sepsis. We used a model of endotoxin-induced acute lung injury to determine whether parenteral ascorbic acid modulates the dysregulated proinflammatory, procoagulant state that leads to lung injury.

Design: C57BL/6 mice were exposed to lethal lipopolysaccharide doses (10 μg/g of body weight) to induce acute lung injury.

Setting: Laboratory investigation.

Subjects: Wild-type C57BL/6 mice.

Interventions: Ascorbic acid or its oxidized form (dehydroascorbic acid) was administered intraperitoneally at 200 mg/kg 30 mins after the lethal lipopolysaccharide dose.

Measurements and Main Results: We quantified survival, lung capillary leak, proinflammatory chemokine expression, and lung microvascular thrombosis. Lipopolysaccharide induced 100% lethality in mice within 28 hrs of exposure and in lung we observed intense neutrophil sequestration, loss of capillary barrier function, exuberant pulmonary inflammation, and extensive microthrombus formation. A time-delayed infusion protocol of both ascorbic acid and dehydroascorbic acid significantly prolonged survival. Both ascorbic acid and dehydroascorbic acid preserved lung architecture and barrier function while attenuating proinflammatory chemokine expression and microvascular thrombosis. Ascorbic acid and dehydroascorbic acid attenuated nuclear factor kappa B activation and normalized coagulation parameters.

Conclusions: Ascorbic acid administered in an interventional manner following lipopolysaccharide infusion attenuates proinflammatory, procoagulant states that induce lung vascular injury in an animal model of sepsis.

© 2011 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins

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