Evidence map›Paper›PMID 22298659›Full record

ReviewPhysiological reviews2012

Hypoxic pulmonary vasoconstriction.

J T Sylvester, Larissa A Shimoda, Philip I Aaronson, Jeremy P T Ward

Erratum issued Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT04998253 (A Randomized Pilot Clinical Trial of the Effects in Oxygenation and Hypoxic Pulmonary Vasoconstriction of Sevoflurane in Patient's Whit ARDS Secondary to Severe Acute Respiratory Syndrome Coronavirus 2), which is not on this map. Cited by 337 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
337citing papers in PubMed, 1 pooled it
22.5field-weighted citation impact, top 1% 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.

NCT04998253 early_phase1completednot on this mapstarted 2020, after this paper: background citation

A Randomized Pilot Clinical Trial of the Effects in Oxygenation and Hypoxic Pulmonary Vasoconstriction of Sevoflurane in Patient's Whit ARDS Secondary to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2)

TypeinterventionalSponsorUnidad Temporal COVID-19 en Centro CitibanamexRan2020 to 2021Enrolled24ConditionsHypoxic Pulmonary Vasoconstriction, Hypoxemia, Acute Respiratory Distress Syndrome, SARS-CoV-2 Acute Respiratory DiseaseArmsEffects in oxygenation and hypoxic pulmonary vasoconstriction
3 · Its place in the literature

Who cites it

337 citing papers in PubMed, 1 synthesis or guideline pooled it, 709 citations in OpenAlex.

  1. Pooled it
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  6. Correlating Pulmonary Hemodynamics With HPMagnetic resonance in medicine · 2026
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277 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

J T SylvesterDivision of Pulmonary & Critical Care Medicine, Department of Medicine, The Johns Hopkins University School ofMedicine, Baltimore, Maryland, USA. jsylv@jhmi.edu
Larissa A Shimoda
Philip I Aaronson
Jeremy P T Ward
Johns Hopkins University · USKing's College London · GB

Funding

Na+/H+ exchange in pulmonary hypertensionR01HL073859 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2003 to 2020
$4.2M
ACUTE PULMONARY ARTERIAL RESPONSES TO HYPOXIAR01HL051912 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SYLVESTER, J T · 1995 to 2004
$2.0M
Chronic hypoxia and pulmonary vascular smooth muscleR01HL067191 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2003 to 2010
$1.9M
Calcium signaling in hypoxic pulmonary vasoconstrictionR01HL075113 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SYLVESTER, J T · 2004 to 2007
$1.6M
British Heart Foundation FS/06/003British Heart Foundation PG/06/151/21995NHLBI NIH HHS HL-51912NHLBI NIH HHS HL-67191NHLBI NIH HHS HL-73859NHLBI NIH HHS HL-75113NHLBI NIH HHS R01 HL051912NHLBI NIH HHS R01 HL067191NHLBI NIH HHS R01 HL073859NHLBI NIH HHS R01 HL075113Wellcome TrustWellcome Trust 078075Wellcome Trust 087776
6 · The paper itself

Abstract

It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

Indexed as

Altitude SicknessCell CommunicationHumansHypertension, PulmonaryHypoxiaInfant, NewbornMuscle, Smooth, VascularPulmonary AlveoliPulmonary Gas ExchangeVasoconstriction

Identifiers

PMID22298659
PMCPMC9469196
OpenAlexW2112861506

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.