Evidence map›Paper›PMID 20383716›Full record

ArticlePflugers Archiv : European journal of physiology2010

Oxygen sensing and conducted vasomotor responses in mouse cremaster arterioles in situ.

Anh Thuc Ngo, Lars Jørn Jensen, Mads Riemann, Niels-Henrik Holstein-Rathlou, Christian Torp-Pedersen

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Inhibition of NaThe Journal of physiology · 2018
    Article
  5. Article
  6. Conducted dilatation to ATP and KActa physiologica (Oxford, England) · 2017
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Spontaneous oscillations in a model for active control of microvessel diameters.Mathematical medicine and biology : a journal of the IMA · 2012
    Article
  13. Article
  14. Review
  15. Nitric oxide signaling in the microcirculation.Critical reviews in biomedical engineering · 2011
    Review
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

5 authors at 2 institutions in 1 country.

Anh Thuc NgoDivision of Renal & Vascular Research, Department of Biomedical Sciences, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark. anhngo@sund.ku.dk
Lars Jørn Jensen
Mads Riemann
Niels-Henrik Holstein-Rathlou
Christian Torp-Pedersen
University of Copenhagen · DKGentofte Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study examines mechanisms by which changes in tissue oxygen tension elicit vasomotor responses and whether localized changes in oxygen tension initiates conducted vasomotor responses in mouse cremaster arterioles. Intravital microscopy was used to visualize the mouse cremaster microcirculation. The cremaster was superfused with Krebs' solution with different oxygen tensions, and a gas exchange chamber was used to induce localized changes in oxygen tension. In arterioles where red blood cells were removed by buffer perfusion, arterioles responded with same magnitudes of vasodilatation (DeltaD = 16.0 +/- 4.9 microm) when changing from high (PO(2) = 242.5 +/- 13.3 mm Hg) to low (PO(2) = 22.5 +/- 4.8 mm Hg) oxygen tension as seen in the intact cremaster circulation (DeltaD = 18.7 +/- 1.0 microm). Blockade of NO synthases by L: -NAME and adenosine receptors by DPCPX had no effects on vasomotor responses to low or high oxygen. Induction of localized low (PO(2) = 23.3 +/- 5.7 mmHg) or high (PO(2) = 300.0 +/- 25.7 mm Hg) oxygen tension caused vasodilatation or -constriction locally and at a site 1,000 microm upstream (distantly). Glibenclamide blocker of ATP-sensitive K(+) channels inhibited vasodilatation and -constriction to low (PO(2) = 16.0 +/- 6.4 mm Hg) and high (PO(2) = 337.4 +/- 12.8 mm Hg) oxygen tension. 1) ATP-sensitive K(+) channels seem to mediate, at least in part, vasodilatation and vasoconstriction to low and high oxygen tension; 2) Red blood cells are not necessary for inducing vasodilatation and vasoconstriction to low or high oxygen tension; 3) localized changes in the oxygen tension cause vasomotor responses, which are conducted upstream along arterioles in mouse cremaster microcirculation.

Indexed as

VasoconstrictionVasodilationAdenosineAdenosine A1 Receptor AntagonistsAdenosine A2 Receptor AntagonistsAnimalsArteriolesCell HypoxiaEnzyme InhibitorsErythrocytesKATP ChannelsMaleMiceMice, Inbred C57BLMicrocirculationMicroscopy, VideoAdenosineAdenosine A1 Receptor AntagonistsAdenosine A2 Receptor AntagonistsEnzyme InhibitorsKATP ChannelsNitric OxideNitric Oxide SynthaseOxygenPotassium Channel BlockersReceptor, Adenosine A1Receptors, Adenosine A2

Identifiers

PMID20383716
OpenAlexW1975890282

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.