Evidence map›Paper›PMID 9327735›Full record

ArticleThe American journal of pathology1997

Pulmonary hemodynamics modify the rat pulmonary artery response to injury. A neointimal model of pulmonary hypertension.

K Okada, Y Tanaka, M Bernstein, W Zhang, G A Patterson, M D Botney

Abstract read
In one paragraph

Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Guideline
  2. Pulmonary vascular changes after lung resection: why less may be more.General thoracic and cardiovascular surgery · 2026
    Review
  3. Review
  4. Pneumonectomy combined with SU5416 or monocrotaline pyrrole does not cause severe pulmonary hypertension in mice.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Animal models of right heart failure.Cardiovascular diagnosis and therapy · 2020
    Review
  13. Article
  14. Drug-induced pulmonary arterial hypertension: a primer for clinicians and scientists.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  15. Article
  16. Characteristics of Pulmonary Vascular Remodeling in a Novel Model of Shunt-Associated Pulmonary Arterial Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  17. Emerging role of angiogenesis in adaptive and maladaptive right ventricular remodeling in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  18. Article
  19. Article
  20. Article
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.

K OkadaDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Y Tanaka
M Bernstein
W Zhang
G A Patterson
M D Botney
Washington University in St. Louis · US

Funding

VASCULAR CELL DIVERSITY IN PULMONARY HYPERTENSIONP01HL029594 · NHLBI · WASHINGTON UNIVERSITY · PI HOLTZMAN, MICHAEL J · 1985 to 2012
$23.8M
LUNG PRESERVATION FOR TRANSPLANTATIONR01HL041281 · NHLBI · WASHINGTON UNIVERSITY · PI PATTERSON, GEORGE ALEXANDER · 1990 to 2006
$1.8M
NHLBI NIH HHS HL29594NHLBI NIH HHS HL41281
6 · The paper itself

Abstract

Hemodynamic factors have profound influences on blood vessels. To test the hypothesis that hemodynamic conditions modify the pattern of remodeling in response to injury, monocrotaline (MCT) injury in Sprague-Dawley rats was followed 1 week later by left pneumonectomy to increase blood flow to the right lung. Right pulmonary artery remodeling in these MCT plus pneumonectomy animals was compared with animals receiving MCT or pneumonectomy alone. Neointimal changes developed in more than 90% of all right lung intra-acinar vessels 5 weeks after MCT injury (4 weeks after pneumonectomy). Neointimal lesions did not develop in untreated animals or in animals receiving MCT or pneumonectomy only. Animals with a neointimal pattern of remodeling developed severe right ventricular hypertrophy (RVH) whereas animals with a medial hypertrophy pattern of remodeling (MCT only) developed moderate RVH compared with control animals. Neointimal lesions and RVH were similar whether injury preceded pneumonectomy or vice versa. To exclude the possibility that neointimal lesions resulted from injury plus post-pneumonectomy compensatory lung growth, rather than injury plus increased flow, a left subclavian-pulmonary artery anastomosis was substituted for pneumonectomy. Neointimal lesions and severe RVH developed in these animals but were not seen in animals receiving either MCT or anastomosis only. These studies demonstrate an important role for hemodynamics in determining the pattern of pulmonary vascular remodeling after injury.

Indexed as

ActinsAnimalsDisease Models, AnimalHemodynamicsHyperplasiaHypertension, PulmonaryHypertrophy, Right VentricularImmunohistochemistryLungMaleMonocrotalinePneumonectomyPulmonary ArteryPulmonary CirculationRatsRats, Sprague-DawleyActinsMonocrotaline

Identifiers

PMID9327735
PMCPMC1858047
OpenAlexW1919041450

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.