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Research: PLEINER and co-workers,
Listed in Issue 84
Abstract
PLEINER and co-workers, Department of Clinical Pharmacology, University of Vienna, Austria, find that high doses of vitamin C reverse endotoxin-induced hyporeactivity to acetylcholine in the forearm.
Background
Acute inflammation causes endothelial vasodilator dysfunction that may be mediated by oxidative stress and thus susceptible to vitamin C.
Methodology
Randomized, double-blinded crossover study on 8 healthy volunteers . Blood flow responses to acetylcholine (which is endothelium-dependent) and to glyceryl trinitrate (which is endothelium- independent) in the forearm were assessed before and after inducing acute inflammation by low doses of Escherichia coli endotoxin (LPS ). The effect of intra-arterial vitamin C at a rate of 24 mg/min or placebo was studied 4 hours after LPS administration. In control experiments, vitamin C was administered without the previous LPS.
Results
LPS caused systemic vasodilation, increased white blood cell count, elevated body temperature, and reduced plasma vitamin C concentrations. The endotoxin decreased the responses of forearm blood flow to acetylcholine by 30% but not to glyceryl trinitride . Vitamin C completely restored the response to acetylcholine, bringing it back to levels comparable to baseline. There was no effect of vitamin C on baseline blood flow or acetylcholine- or glyceryl trinitrate-induced vasodilation in control subjects .
Conclusion
The data demonstrate that impaired endothelial vasodilation caused by E.coli endotoxemia can be counteracted by high doses of antioxidant in vivo. Oxidative stress may therefore play an important role in the pathogenesis of endothelial dysfunction during inflammation.
References
Pleiner J, Mittermayer F, Schaller G, MacAllister RJ, Wolzt M. High doses of vitamin C reverse E.coli endotoxin-induced hyporeactivity to acetylcholine in the human forearm. Circulation 106 (12): 1460-1464, Sep 2002.