Evidence map›Paper›PMID 19164779›Full record

ArticleStroke2009

Roles of glia limitans astrocytes and carbon monoxide in adenosine diphosphate-induced pial arteriolar dilation in newborn pigs.

Alie Kanu, Charles W Leffler

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Neurovascular signaling in the brain and the pathological consequences of hypertension.American journal of physiology. Heart and circulatory physiology · 2014
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Glutamate-induced calcium signals stimulate CO production in piglet astrocytes.American journal of physiology. Heart and circulatory physiology · 2011
    Article
  15. Carbon monoxide as an endogenous vascular modulator.American journal of physiology. Heart and circulatory physiology · 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

2 authors at 1 institution in 1 country.

Alie KanuLaboratory for Research in Neonatal Physiology, Department of Physiology, University of Tennessee Health Science Center, Memphis, Tenn., USA.
Charles W Leffler
University of Tennessee Health Science Center · US

Funding

STUDIES OF THE CONTROL OF NEONATAL CIRCULATIONR01HL034059 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI PARFENOVA, HELENA · 1985 to 2016
$5.9M
CARBON MONOXIDE IN NEWBORN CEREBRAL CIRCULATIONR37HL042851 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEFFLER, CHARLES W. · 2000 to 2009
$3.5M
NHLBI NIH HHS R01 HL034059NHLBI NIH HHS R37 HL042851
6 · The paper itself

Abstract

background and purposeAstrocytes, neurons, and microvessels together form a neurovascular unit allowing blood flow to match neuronal activity. Adenosine diphosphate (ADP) is an important signaling molecule in the brain, and dilation in response to ADP is astrocyte-dependent in rats and newborn pigs. Carbon monoxide (CO), produced endogenously by catabolism of heme to CO, iron, and biliverdin via heme oxygenase, is an important cell-signaling molecule in the neonatal cerebral circulation. We hypothesize ADP stimulates CO production by glia limitans astrocytes and that this CO causes pial arteriolar dilation.

methodsExperiments were performed using anesthetized piglet with closed cranial windows, and freshly isolated piglet astrocytes and microvessels. Astrocyte injury was caused by topical application of L-2-alpha aminoadipic acid (2 mmol/L, 5 hours). Cerebrospinal fluid was collected from under the cranial windows for measurement of ADP-stimulated CO production. CO was measured by gas chromatography-mass spectroscopy analysis.

resultsBefore, but not after, astrocyte injury in vivo, topical ADP stimulated both CO production and dilation of pial arterioles. Astrocyte injury did not block dilation to isoproterenol or bradykinin. Chromium mesoporphyrin, an inhibitor of heme oxygenase, also prevented the ADP-induced increase in cerebrospinal fluid CO and pial arteriolar dilation caused by ADP, but not dilation to sodium nitroprusside. ADP also increased CO production by freshly isolated piglet astrocytes and cerebral microvessels, although the increase was smaller in the microvessels.

conclusionsThese data suggest that glia limitans astrocytes use CO as a gasotransmitter to cause pial arteriolar dilation in response to ADP.

Indexed as

Vasodilator Agents2-Aminoadipic AcidAdenosine DiphosphateAdrenergic beta-AgonistsAnimalsAnimals, NewbornAstrocytesCapillariesCarbon MonoxideCerebral ArteriesExcitatory Amino Acid AntagonistsIn Vitro TechniquesIsoproterenolNeurogliaNitroprussideSwine2-Aminoadipic AcidAdenosine DiphosphateAdrenergic beta-AgonistsCarbon MonoxideExcitatory Amino Acid AntagonistsIsoproterenolNitroprussideVasodilator Agents

Identifiers

PMID19164779
PMCPMC2647584
OpenAlexW2121297924

What OpenQuestion holds

Textmetadata
LicenceTDM
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.