Evidence map›Paper›PMID 20418473›Full record

ReviewCardiovascular research2010

Vascular permeability modulation at the cell, microvessel, or whole organ level: towards closing gaps in our knowledge.

Fitz-Roy E Curry, Roger H Adamson

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
9.7field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 157 citations in OpenAlex.

  1. Trial
  2. Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Leveraging avidin-biotin interaction to quantify permeability property of microvessels-on-a-chip networks.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

16 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Fitz-Roy E CurryDepartment of Physiology and Membrane Biology, School of Medicine, University of California, 1 Shields Avenue, Davis, CA 95616, USA. fecurry@ucdavis.edu
Roger H Adamson
University of California, Davis · US

Funding

NEW APPROACH TO ENDOTHELIAL CLEFT STRUCTURER01HL044485 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI CURRY, FITZ-ROY E · 1991 to 2010
$4.0M
WATER AND SOLUTE TRANSPORT ACROSS CAPILLARY ENDOTHELIUMR01HL028607 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI CURRY, FITZ-ROY E · 1985 to 2014
$3.9M
TRANSPORT ACROSS CAPILLARY ENDOTHELIUMR37HL028607 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI CURRY, FITZ-ROY E · 1992 to 2001
$504k
NHLBI NIH HHS HL28607NHLBI NIH HHS HL44485
6 · The paper itself

Abstract

Multiple processes modulate net blood-to-tissue exchange in a microvascular unit in normal and pathophysiological conditions. These include mechanisms that control the number and type of microvessels perfused, the balance of adhesion and contractile forces that determine the conductance of the spaces between endothelial cells to water and solutes, the pressure and chemical potential gradients determining the driving forces through these conductive pathways, and the organization of barriers to macromolecules in the endothelial glycocalyx. Powerful methods are available to investigate these mechanisms at the levels of cultured endothelial monolayers, isolated microvessels, and the microvascular units within intact organs. Here we focus on current problems that limit the integration of our knowledge of mechanisms investigated in detail at the cellular level into a more complete understanding of modulation of blood-to-tissue exchange in whole organs when the endothelial barrier is exposed to acute and more long-term inflammatory conditions. First, we review updated methods, applicable in mouse models of vascular permeability regulation, to investigate both acute and long-term changes in permeability. Methods to distinguish tracer accumulation due to change in perfusion from real increases in extravascular accumulation are emphasized. The second part of the review compares normal and increased permeability in individually perfused venular microvessels and endothelial cell monolayers. The heterogeneity of endothelial cell phenotypes in the baseline state and after exposure to injury and inflammatory conditions is emphasized. Lastly, we review new approaches to investigation of the glycocalyx barrier properties in cultured endothelial monolayers and in whole-body investigations.

Indexed as

Capillary PermeabilityAnimalsBody FluidsEdemaEndothelium, VascularGlycocalyxHumansInflammationInflammation MediatorsMiceMicrovesselsModels, AnimalModels, CardiovascularOsmotic PressureRegional Blood FlowThrombinInflammation MediatorsThrombin

Identifiers

PMID20418473
PMCPMC2895542
OpenAlexW2162303223

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.