Evidence map›Paper›PMID 24713530›Full record

ArticleStroke2014

Dichotomous effects of chronic intermittent hypoxia on focal cerebral ischemic injury.

Katherine A Jackman, Ping Zhou, Giuseppe Faraco, Pablo M Peixoto, Christal Coleman, Henning U Voss, Virginia Pickel, Giovanni Manfredi, Costantino Iadecola

Abstract read
In one paragraph

Article in Stroke, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Review
  2. Review
  3. Tau Protein Alterations Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2024
    Review
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  5. Review
  6. Article
  7. Review
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  9. Article
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  11. Article
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  13. Endothelial S1PCirculation research · 2021
    Article
  14. Review
  15. Article
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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

9 authors.

Katherine A JackmanFrom the Feil Family Brain and Mind Research Institute (K.A.J., P.Z., G.F., P.M.P., C.C., V.P., G.M., C.I.) and Department of Radiology (H.U.V.), Weill Cornell Medical College, New York; and Department of Natural Sciences, Baruch College, City University of New York (P.M.P.).
Ping Zhou
Giuseppe Faraco
Pablo M Peixoto
Christal Coleman
Henning U Voss
Virginia Pickel
Giovanni Manfredi
Costantino Iadecola

Funding

Radiotelemetry CoreP01HL096571 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DAVISSON, ROBIN L · 2009 to 2013
$8.8M
CHRONIC INTERMITTENT HYPOXIA, NEUROVASCULAR DYSFUNCTION AND STROKER01NS073666 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 2011 to 2015
$1.8M
NHLBI NIH HHS P01 HL096571NHLBI NIH HHS P01-HL96571NINDS NIH HHS R01 NS073666NINDS NIH HHS R01-NS73666
6 · The paper itself

Abstract

background and purposeObstructive sleep apnea, a condition associated with chronic intermittent hypoxia (CIH), carries an increased risk of stroke. However, CIH has been reported to either increase or decrease brain injury in models of focal cerebral ischemia. The factors determining the differential effects of CIH on ischemic injury and their mechanisms remain unclear. Here, we tested the hypothesis that the intensity of the hypoxic challenge determines the protective or destructive nature of CIH by modulating mitochondrial resistance to injury.

methodsMale C57Bl/6J mice were exposed to CIH with 10% or 6% O2 for ≤35 days and subjected to transient middle cerebral artery occlusion. Motor deficits and infarct volume were assessed 3 days later. Intraischemic cerebral blood flow was measured by laser-Doppler flowmetry and resting cerebral blood flow by arterial spin labeling MRI. Ca2+-induced mitochondrial depolarization and reactive oxygen species production were evaluated in isolated brain mitochondria.

resultsWe found that 10% CIH is neuroprotective, whereas 6% CIH exacerbates tissue damage. No differences in resting or intraischemic cerebral blood flow were observed between 6% and 10% CIH. However, 10% CIH reduced, whereas 6% CIH increased, mitochondrial reactive oxygen species production and susceptibility to Ca2+-induced depolarizations.

conclusionsThe influence of CIH on the ischemic brain is dichotomous and can be attributed, in part, to changes in the mitochondrial susceptibility to injury. The findings highlight a previously unappreciated complexity in the effect of CIH on the brain, which needs to be considered in evaluating the neurological effect of conditions associated with cyclic hypoxia.

Indexed as

AnimalsCerebrovascular CirculationChronic DiseaseDisease Models, AnimalHypoxiaInfarction, Middle Cerebral ArteryLaser-Doppler FlowmetryMaleMiceMice, Inbred C57BLMitochondriaReactive Oxygen SpeciesReactive Oxygen Speciesfree radicalsmitochondriasleep apnea syndromesstroke

Identifiers

PMID24713530
PMCPMC4006286

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Registered trials

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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.