Evidence map›Paper›PMID 28755882›Full record

ArticleThe Journal of thoracic and cardiovascular surgery2017

Pulmonary hypertension due to left heart disease causes intrapulmonary venous arterialization in rats.

Yoshitaka Fujimoto, Takashi Urashima, Fumie Kawachi, Toru Akaike, Yoichiro Kusakari, Hiroyuki Ida, Susumu Minamisawa

Open access · bronzeAbstract read
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In one paragraph

Article in The Journal of thoracic and cardiovascular surgery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  7. Animal models of pulmonary hypertension due to left heart disease.Animal models and experimental medicine · 2022
    Review
  8. Review
  9. Longitudinal Impact of WTC Dust Inhalation on Rat Cardiac Tissue Transcriptomic Profiles.International journal of environmental research and public health · 2022
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Yoshitaka FujimotoDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan; Department of Pediatrics, The Jikei University School of Medicine, Tokyo, Japan.
Takashi UrashimaDepartment of Pediatrics, The Jikei University School of Medicine, Tokyo, Japan.
Fumie KawachiDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan; Department of Pediatrics, The Jikei University School of Medicine, Tokyo, Japan.
Toru AkaikeDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Yoichiro KusakariDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Hiroyuki IdaDepartment of Pediatrics, The Jikei University School of Medicine, Tokyo, Japan.
Susumu MinamisawaDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan. Electronic address: sminamis@jikei.ac.jp.
Jikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveA rat model of left atrial stenosis-associated pulmonary hypertension due to left heart diseases was prepared to elucidate its mechanism.

methodsFive-week-old Sprague-Dawley rats were randomly divided into 2 groups: left atrial stenosis and sham-operated control. Echocardiography was performed 2, 4, 6, and 10 weeks after surgery, and cardiac catheterization and organ excision were subsequently performed at 10 weeks after surgery.

resultsLeft ventricular inflow velocity, measured by echocardiography, significantly increased in the left atrial stenosis group compared with that in the sham-operated control group (2.2 m/s, interquartile range [IQR], 1.9-2.2 and 1.1 m/s, IQR, 1.1-1.2, P < .01), and the right ventricular pressure-to-left ventricular systolic pressure ratio significantly increased in the left atrial stenosis group compared with the sham-operated control group (0.52, IQR, 0.54-0.60 and 0.22, IQR, 0.15-0.27, P < .01). The right ventricular weight divided by body weight was significantly greater in the left atrial stenosis group than in the sham-operated control group (0.54 mg/g, IQR, 0.50-0.59 and 0.39 mg/g, IQR, 0.38-0.43, P < .01). Histologic examination revealed medial hypertrophy of the pulmonary vein was thickened by 1.6 times in the left atrial stenosis group compared with the sham-operated control group. DNA microarray analysis and real-time polymerase chain reaction revealed that transforming growth factor-β mRNA was significantly elevated in the left atrial stenosis group. The protein levels of transforming growth factor-β and endothelin-1 were increased in the lung of the left atrial stenosis group by Western blot analyses.

conclusionsWe successfully established a novel, feasible rat model of pulmonary hypertension due to left heart diseases by generating left atrial stenosis. Although pulmonary hypertension was moderate, the pulmonary hypertension due to left heart diseases model rats demonstrated characteristic intrapulmonary venous arterialization and should be used to further investigate the mechanism of pulmonary hypertension due to left heart diseases.

Indexed as

Heart AtriaHeart VentriclesHypertension, PulmonaryPulmonary VeinsAnimalsConstriction, PathologicDisease Models, AnimalEchocardiographyPulmonary CirculationRatsRats, Sprague-DawleyVentricular Dysfunction, Leftpulmonary hypertension due to left heart diseasepulmonary veinrat model

Identifiers

PMID28755882
OpenAlexW2724174606

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Registered trials

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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.