Evidence map›Paper›PMID 25340330›Full record

ArticleChest2015

Effect of acute arteriolar vasodilation on capacitance and resistance in pulmonary arterial hypertension.

John H Newman, Evan L Brittain, Ivan M Robbins, Anna R Hemnes

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Chest, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 24 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

4 authors at 1 institution in 1 country.

John H NewmanPulmonary Circulation Center, Divisions of Pulmonary and Critical Care Medicine and Cardiology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN. Electronic address: john.newman@vanderbilt.edu.
Evan L BrittainPulmonary Circulation Center, Divisions of Pulmonary and Critical Care Medicine and Cardiology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
Ivan M RobbinsPulmonary Circulation Center, Divisions of Pulmonary and Critical Care Medicine and Cardiology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
Anna R HemnesPulmonary Circulation Center, Divisions of Pulmonary and Critical Care Medicine and Cardiology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
Vanderbilt University · US

Funding

Sex Hormones in Pulmonary Arterial HypertensionP01HL108800 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI NEWMAN, JOHN HUGHES · 2012 to 2021
$22.0M
NHLBI NIH HHS P01 HL108800PHS HHS P01 108800-01
6 · The paper itself

Abstract

backgroundPulmonary vascular capacitance (PVC) is reduced in pulmonary arterial hypertension (PAH). In normal lung, PVC is largely a function of vascular compliance. In PAH, increased pulmonary vascular resistance (PVR) arises from the arterioles. PVR and PVC share pressure and volume variables. The dependency between the two qualities of the vascular bed is unclear in a state of intense vasoconstriction.

methodsWe compared PVC and PVR before and during nitric oxide (NO) inhalation during right-sided heart catheterization in eight NO-responsive patients with PAH. NO only directly affects tone in parenchymal vessels.

resultsDuring NO inhalation, pulmonary arterial systolic pressure decreased, 80 ± 20 SD to 48 ± 20 mm Hg, and stroke volume increased, 62 ± 19 mL to 86 ± 24 mL (P < .01). PVR dropped from 10 ± 4.4 Wood units to 4.7 ± 2.2 Wood units (P < .012), and PVC increased from 1.4 ± 1.1 mL/mm Hg to 3.2 ± 1.8 mL/mm Hg (P < .018). The magnitude of PVR drop was 57% ± 6% and the decrease in 1/PVC was 54% ± 14% (P = not significant).

conclusionsIn vasoresponsive PAH, PVC is a function of the pressure response of the vasoconstricted arterioles to stroke volume. Immediately upon vasodilation, the capacitance increases markedly. The compliance vessels are, thus, the same as the resistance vessels. The immediate reduction in pulmonary arterial pressure during NO inhalation suggests that large vessel remodeling is not a major contributor to systolic pressure in these patients.

Indexed as

Nitric OxideAdministration, InhalationCardiac CatheterizationEndothelium-Dependent Relaxing FactorsFemaleHumansHypertension, PulmonaryMaleMiddle AgedPulmonary Wedge PressureStroke VolumeVascular RemodelingVascular ResistanceVasodilationVentricular Function, RightEndothelium-Dependent Relaxing FactorsNitric Oxide

Identifiers

PMID25340330
PMCPMC4388116
OpenAlexW2104573321

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.