Evidence map›Paper›PMID 20139112›Full record

ArticleCardiovascular research2010

Oxidative stress contributes to methamphetamine-induced left ventricular dysfunction.

Kevin C Lord, Sylvia K Shenouda, Elizabeth McIlwain, Dimitrios Charalampidis, Pamela A Lucchesi, Kurt J Varner

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 74 citations in OpenAlex.

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  12. Cardiovascular magnetic resonance imaging characteristics in patients with methamphetamine-associated cardiomyopathy.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2022
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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 3 institutions in 1 country.

Kevin C LordDepartment of Pharmacology and Experimental Therapeutics, Louisiana State University Health Science Center, 1901 Perdido Street, New Orleans, LA 70112, USA.
Sylvia K Shenouda
Elizabeth McIlwain
Dimitrios Charalampidis
Pamela A Lucchesi
Kurt J Varner
Louisiana State University Health Sciences Center New Orleans · USNationwide Children's Hospital · USUniversity of New Orleans · US

Funding

VASCULAR SMOOTH MUSCLE PLASTICITY IN NITRIC OXIDEP20RR018766 · NCRR · LSU HEALTH SCIENCES CENTER · PI SUKHANOV, SERGIY · 2003 to 2011
$18.5M
Reactive Inflammatory Species in Heart FailureR01HL063318 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUCCHESI, PAMELA A · 1999 to 2006
$2.1M
NCRR NIH HHS P20 RR18766NHLBI NIH HHS HL63318
6 · The paper itself

Abstract

aimsOur aim was to test the hypothesis that the repeated, binge administration of methamphetamine would produce oxidative stress in the myocardium leading to structural remodeling and impaired left ventricular function. METHODS AND

resultsEchocardiography and Millar pressure-volume catheters were used to monitor left ventricular structure and function in rats subjected to four methamphetamine binges (3 mg/kg, iv for 4 days, separated by a 10-day drug-free period). Hearts from treated and control rats were used for histological or proteomic analysis. When compared with saline treatment, four methamphetamine binges produced eccentric left ventricular hypertrophy. The drug also significantly impaired systolic function (decreased fractional shortening, ejection fraction, and adjusted maximal power) and produced significant diastolic dysfunction (increased -dP/dt and tau). Dihydroethedium staining showed that methamphetamine significantly increased (285%) the levels of reactive oxygen species in the left ventricle. Treatment with methamphetamine also resulted in the tyrosine nitration of myofilament (desmin, myosin light chain) and mitochondrial (ATP synthase, NADH dehydrogenase, cytochrome c oxidase, prohibitin) proteins. Treatment with the superoxide dismutase mimetic, tempol in the drinking water prevented methamphetamine-induced left ventricular dilation and systolic dysfunction; however, tempol (2.5 mM) did not prevent the diastolic dysfunction. Tempol significantly reduced, but did not eliminate dihydroethedium staining in the left ventricle, nor did it prevent the tyrosine nitration of mitochondrial and contractile proteins.

conclusionThis study shows that oxidative stress plays a significant role in mediating methamphetamine-induced eccentric left ventricular dilation and systolic dysfunction.

Indexed as

Oxidative StressVentricular Function, LeftVentricular RemodelingActin CytoskeletonAnimalsAntioxidantsCardiac CatheterizationCyclic N-OxidesDisease Models, AnimalMaleMethamphetamineMitochondrial ProteinsMyocardial ContractionMyocardiumRatsRats, Sprague-Dawley3-nitrotyrosineAntioxidantsCyclic N-OxidesMethamphetamineMitochondrial ProteinsSpin LabelstempolTyrosine

Identifiers

PMID20139112
PMCPMC2883898
OpenAlexW2144916780

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.