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Research Article Free access | 10.1172/JCI1155

L-2-Oxothiazolidine-4-carboxylic acid reverses endothelial dysfunction in patients with coronary artery disease.

J A Vita, B Frei, M Holbrook, N Gokce, C Leaf, and J F Keaney Jr

Evans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu

Find articles by Vita, J. in: JCI | PubMed | Google Scholar

Evans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu

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Evans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu

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Evans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu

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Evans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu

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Evans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu

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Published March 15, 1998 - More info

Published in Volume 101, Issue 6 on March 15, 1998
J Clin Invest. 1998;101(6):1408–1414. https://doi.org/10.1172/JCI1155.
© 1998 The American Society for Clinical Investigation
Published March 15, 1998 - Version history
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Abstract

The effective action of endothelium-derived nitric oxide (EDNO) is impaired in patients with atherosclerosis. This impairment has been attributed in part to increased vascular oxidative stress. EDNO action is improved by administration of ascorbic acid, a water-soluble antioxidant. Ascorbic acid is a potent free-radical scavenger in plasma, and also regulates intracellular redox state in part by sparing cellular glutathione. We specifically investigated the role of intracellular redox state in EDNO action by examining the effect of L-2-oxo-4-thiazolidine carboxylate (OTC) on EDNO-dependent, flow-mediated dilation in a randomized double-blind placebo-controlled study of patients with angiographically proven coronary artery disease. OTC augments intracellular glutathione by providing substrate cysteine for glutathione synthesis. Brachial artery flow-mediated dilation was examined with high-resolution ultrasound before and after oral administration of 4.5 g of OTC or placebo in 48 subjects with angiographically documented coronary artery disease. Placebo treatment produced no change in flow-mediated dilation (7.0+/-3.9% vs. 7.2+/-3.7%), whereas OTC treatment was associated with a significant improvement in flow-mediated dilation (6.6+/-4.4% vs. 11.0+/-6.3%; P = 0.005). OTC had no effect on arterial dilation to nitroglycerin, systemic blood pressure, heart rate, or reactive hyperemia. These data suggest that augmenting cellular glutathione levels improves EDNO action in human atherosclerosis. Cellular redox state may be an important regulator of EDNO action, and is a potential target for therapy in patients with coronary artery disease.

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  • Version 1 (March 15, 1998): No description

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