Evidence map›Paper›PMID 29411543›Full record

ArticlePhysiological reports2018

Lumped-parameter models of the pulmonary vasculature during the progression of pulmonary arterial hypertension.

Jesse W Gerringer, Julie C Wagner, Daniela Vélez-Rendón, Daniela Valdez-Jasso

Abstract read
In one paragraph

Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Guidelines for mechanistic modeling and analysis in cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

4 authors.

Jesse W GerringerDepartment of Bioengineering, University of Illinois at Chicago, Chicago, Illinois.
Julie C WagnerDepartment of Bioengineering, University of Illinois at Chicago, Chicago, Illinois.
Daniela Vélez-RendónDepartment of Bioengineering, University of Illinois at Chicago, Chicago, Illinois.
Daniela Valdez-JassoDepartment of Bioengineering, University of Illinois at Chicago, Chicago, Illinois.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A longitudinal study of monocrotaline-induced pulmonary arterial hypertension (PAH) was carried out in Sprague-Dawley rats to investigate the changes in impedance (comprising resistance and compliance) produced by elevated blood pressure. Using invasively measured blood flow as an input, blood pressure was predicted using 3- and 4-element Windkessel (3WK, 4WK) type lumped-parameter models. Resistance, compliance, and inductance model parameters were obtained for the five different treatment groups via least-squares errors. The treated animals reached levels of hypertension, where blood pressure increased two folds from control to chronic stage of PAH (mean pressure went from 24 ± 5 to 44 ± 6 mmHg, P < 0.0001) but blood flow remained overall unaffected. Like blood pressure, the wave-reflection coefficient significantly increased at the advanced stage of PAH (0.26 ± 0.09 to 0.52 ± 0.09, P < 0.0002). Our modeling efforts revealed that resistances and compliance changed during the disease progression, where changes in compliance occur before the changes in resistance. However, resistance and compliance are not directly inversely related. As PAH develops, resistances increase nonlinearly (R

Indexed as

Models, CardiovascularAnimalsHemodynamicsHypertension, PulmonaryMaleMonocrotalinePulmonary ArteryRatsRats, Sprague-DawleyMonocrotalineImpedancemathematical modelingmonocrotalineparameter estimationpulmonary arterial hypertensionWindkessel models

Identifiers

PMID29411543
PMCPMC5901176

What OpenQuestion holds

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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.