Evidence map›Paper›PMID 9502783›Full record

Trial reportThe Journal of clinical investigation1998

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, J F Keaney

Open access · greenAbstract readClinical TrialRandomized Controlled Trial
In one paragraph

Trial report in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
8.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 139 citations in OpenAlex.

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  3. Effect of thiol antioxidant on body fat and insulin reactivity.Journal of molecular medicine (Berlin, Germany) · 2004
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

J A VitaEvans Memorial Department of Medicine, Cardiology Section and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jvita@acs.bu.edu
B Frei
M Holbrook
N Gokce
C Leaf
J F Keaney
Boston University · US

Funding

CORONARY REACTIVITY AND OXIDATIVE STRESSR01HL053398 · NHLBI · BOSTON MEDICAL CENTER · PI VITA, JOSEPH A. · 1995 to 1999
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VITAMIN C, GLUTATHIONE, AND ENDOTHELIAL CELL FUNCTIONR01HL056170 · NHLBI · OREGON STATE UNIVERSITY · PI FREI, BALZ B · 1996 to 1999
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NHLBI NIH HHS HL03195NHLBI NIH HHS HL53398NHLBI NIH HHS HL56170
6 · The paper itself

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.

Indexed as

Administration, OralAgedArteriosclerosisBlood Flow VelocityBlood GlucoseBlood PressureCholesterolCoronary DiseaseCysteineDouble-Blind MethodEndothelium, VascularFemaleGlutathioneHeart RateHumansHyperemia2-oxothiazolidine-4-carboxylic acidBlood GlucoseCholesterolCysteineGlutathioneNitric OxideNitroglycerinPyrrolidonecarboxylic AcidThiazolesThiazolidinesTriglycerides

Identifiers

PMID9502783
PMCPMC508696
OpenAlexW2020016552

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.