Evidence map›Paper›PMID 28491305›Full record

ArticleSAGE open medicine2017

Effects of carvedilol on structural and functional outcomes and plasma biomarkers in the mouse transverse aortic constriction heart failure model.

Caryn Hampton, Raymond Rosa, Daphne Szeto, Gail Forrest, Barry Campbell, Richard Kennan, Shubing Wang, Chin-Hu Huang, Loise Gichuru, Xiaoli Ping and 4 more

Open access · goldAbstract read
In one paragraph

Article in SAGE open medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

14 authors at 1 institution in 1 country.

Caryn HamptonIn Vivo Pharmacology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Raymond RosaIn Vivo Pharmacology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Daphne SzetoIn Vivo Pharmacology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Gail ForrestIn Vivo Pharmacology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Barry CampbellTranslational Imaging Biomarkers, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Richard KennanTranslational Imaging Biomarkers, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Shubing WangBiometrics Research, Merck Research Laboratories (MRL), Rahway, NJ, USA.
Chin-Hu HuangCardiometabolic Disease Biology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Loise GichuruLaboratory Animal Resources, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Xiaoli PingLaboratory Animal Resources, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Xiaolan ShenLaboratory Animal Resources, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Kersten SmallCardiometabolic Disease Biology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Jeffrey MadwedCardiometabolic Disease Biology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Joseph J LynchIn Vivo Pharmacology, Merck Research Laboratories (MRL), Kenilworth, NJ, USA.
Merck & Co., Inc., Rahway, NJ, USA (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDespite the widespread use of the mouse transverse aortic constriction heart failure model, there are no reports on the characterization of the standard-of-care agent carvedilol in this model.

methodsLeft ventricular pressure overload was produced in mice by transverse aortic constriction between the innominate and left common carotid arteries. Carvedilol was administered at multiple dose levels (3, 10 and 30 mg/kg/day

resultsCarvedilol treatment in transverse aortic constriction mice significantly decreased heart rate and left ventricular dP/dt (max) at all dose levels consistent with β-adrenoceptor blockade. The middle dose of carvedilol significantly decreased left ventricular weight, whereas the higher dose decreased total heart, left and right ventricular weight and wet lung weight compared to untreated transverse aortic constriction mice. The higher dose of carvedilol significantly increased cardiac performance as measured by ejection fraction and fractional shortening and decreased left ventricular end systolic volume consistent with the beneficial effect on cardiac function. End-study plasma sST-2 and Gal-3 levels did not differ among sham, transverse aortic constriction control and transverse aortic constriction carvedilol groups. Plasma b

conclusionA comparison of carvedilol hemodynamic and structural effects in the mouse transverse aortic constriction model versus clinical use indicates a strong agreement in effect profiles preclinical versus clinical, providing important translational validation for this widely used animal model. The present plasma brain natriuretic peptide biomarker findings support the measurement of plasma natriuretic peptides in the mouse transverse aortic constriction model to extend the translational utility of the model.

Indexed as

cardiovascularcarvedilolHeart failuretransverse aortic constriction

Identifiers

PMID28491305
PMCPMC5406154
OpenAlexW2598114468

What OpenQuestion holds

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LicenceCC BY-NC
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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.