Evidence map›Paper›PMID 24754626›Full record

ArticleAlcoholism, clinical and experimental research2014

Oxidative stress and autonomic dysregulation contribute to the acute time-dependent myocardial depressant effect of ethanol in conscious female rats.

Badr M Ibrahim, Ming Fan, Abdel A Abdel-Rahman

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  14. Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis.The international journal of biochemistry & cell biology · 2017
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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

3 authors at 1 institution in 1 country.

Badr M IbrahimDepartment of Pharmacology and Toxicology (BMI, MF, AAR-R), Brody School of Medicine, East Carolina University, Greenville, North Carolina.
Ming Fan
Abdel A Abdel-Rahman
East Carolina University · US

Funding

Sex/estrogen-dependent vulnerability to alcohol-evoked cardiotoxicity: Role of circadian rhythm regulated enzymesR01AA014441 · NIAAA · EAST CAROLINA UNIVERSITY · PI ABDEL-RAHMAN, ABDEL A · 2004 to 2022
$5.2M
NIAAA NIH HHS 2R01 AA14441-06NIAAA NIH HHS R01 AA014441
6 · The paper itself

Abstract

backgroundThe molecular mechanisms of the acute hypotensive and indirectly assessed cardiac depressant effect of ethanol (EtOH)-evoked myocardial depression and hypotension in female rats are not known. We tested the hypothesis that a time-dependent myocardial depression caused by EtOH is initiated by its direct and indirect (cardiac vagal dominance) effects and is exacerbated by gradual development of oxidative stress.

methodsIn conscious female rats, we directly measured left ventricular developed pressure (LVDP), the maximal rise of ventricular pressure over time (dP/dtmax ), blood pressure (BP), heart rate (HR), and sympathovagal activity following intragastric EtOH (1 g/kg) or water over 90 minutes. Catalytic activity of acetaldehyde (ACA)-generating (alcohol dehydrogenase [ADH] and catalase) and eliminating aldehyde dehydrogenase [ALDH2] enzymes along with mediators of oxidative stress were measured in myocardial tissues collected at 30, 60, or 90 minutes after EtOH or water.

resultsEtOH reduced myocardial function (LVDP and dP/dtmax ) within 5 to 10 minutes before the steady fall in BP in conscious proestrus rats. Further, EtOH shifted the sympathovagal balance, analyzed by spectral analysis of high frequency and low frequency of interbeat intervals, toward vagal dominance. Prior vagal blockade (atropine) or antioxidant (tempol) treatment attenuated EtOH-evoked myocardial depression and hypotension. Ex vivo studies revealed time-dependent: (i) enhancement of ADH, but not ALDH2 activity (indicative of elevated ACA levels), (ii) increases in phosphorylated Akt and ERK1/2, NADPH-oxidase activity, reactive oxygen species, malondialdehyde, and 4-hydroxy-2-nonenal-modified proteins. These molecular responses along with reduced myocardial catalase activity were most evident at 90 minutes post-EtOH when the reductions in cardiac function and BP reached their nadir.

conclusionsVagal dominance and time-dependent myocardial oxidative stress along with the accumulation of cardiotoxic aldehydes mediate EtOH-evoked myocardial dysfunction and hypotension in conscious proestrus female rats.

Indexed as

Aldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAnimalsAutonomic Nervous SystemBlood PressureCatalaseEthanolFemaleHeartHeart RateMitochondrial ProteinsMyocardial ContractionMyocardiumOxidative StressRatsRats, Sprague-DawleyAldehyde DehydrogenaseAldehyde Dehydrogenase, MitochondrialAldh2 protein, ratCatalaseEthanolMitochondrial ProteinsEthanolFemale RatsHypotensionMyocardial DysfunctionReactive Oxygen Species

Identifiers

PMID24754626
PMCPMC3999510
OpenAlexW2005598030

What OpenQuestion holds

Textmetadata
LicenceTDM
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.