Evidence map›Paper›PMID 26676248›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

Hypoxemia, oxygen content, and the regulation of cerebral blood flow.

Ryan L Hoiland, Anthony R Bain, Mathew G Rieger, Damian M Bailey, Philip N Ainslie

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 5 pooled it
6.1field-weighted citation impact, top 3% 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

125 citing papers in PubMed, 5 syntheses or guidelines pooled it, 245 citations in OpenAlex.

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  20. Equip your vehicle for the right terrain: Using features of local pathology to guide engineering of targeted drug delivery systems.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Review

65 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

5 authors at 3 institutions in 2 countries.

Ryan L HoilandCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan Campus, Kelowna, British Columbia, Canada; and ryanleohoiland@gmail.com.
Anthony R BainCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan Campus, Kelowna, British Columbia, Canada; and.
Mathew G RiegerCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan Campus, Kelowna, British Columbia, Canada; and.
Damian M BaileyNeurovascular Research Laboratory, Research Institute of Science and Health, University of South Wales, Glamorgan, United Kingdom.
Philip N AinslieCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan Campus, Kelowna, British Columbia, Canada; and Neurovascular Research Laboratory, Research Institute of Science and Health, University of South Wales, Glamorgan, United Kingdom.
Okanagan University College · CAUniversity of British Columbia · CAUniversity of South Wales · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review highlights the influence of oxygen (O2) availability on cerebral blood flow (CBF). Evidence for reductions in O2 content (CaO2 ) rather than arterial O2 tension (PaO2 ) as the chief regulator of cerebral vasodilation, with deoxyhemoglobin as the primary O2 sensor and upstream response effector, is discussed. We review in vitro and in vivo data to summarize the molecular mechanisms underpinning CBF responses during changes in CaO2 . We surmise that 1) during hypoxemic hypoxia in healthy humans (e.g., conditions of acute and chronic exposure to normobaric and hypobaric hypoxia), elevations in CBF compensate for reductions in CaO2 and thus maintain cerebral O2 delivery; 2) evidence from studies implementing iso- and hypervolumic hemodilution, anemia, and polycythemia indicate that CaO2 has an independent influence on CBF; however, the increase in CBF does not fully compensate for the lower CaO2 during hemodilution, and delivery is reduced; and 3) the mechanisms underpinning CBF regulation during changes in O2 content are multifactorial, involving deoxyhemoglobin-mediated release of nitric oxide metabolites and ATP, deoxyhemoglobin nitrite reductase activity, and the downstream interplay of several vasoactive factors including adenosine and epoxyeicosatrienoic acids. The emerging picture supports the role of deoxyhemoglobin (associated with changes in CaO2 ) as the primary biological regulator of CBF. The mechanisms for vasodilation therefore appear more robust during hypoxemic hypoxia than during changes in CaO2 via hemodilution. Clinical implications (e.g., disorders associated with anemia and polycythemia) and future study directions are considered.

Indexed as

Cerebrovascular CirculationVasodilationAcclimatizationAdenosine TriphosphateAltitudeAltitude SicknessAnimalsCerebral ArteriesHemodilutionHemoglobinsHomeostasisHumansHypoxiaNitric OxideOxygenSignal TransductionAdenosine TriphosphatedeoxyhemoglobinHemoglobinsNitric OxideOxygenadenosine triphosphatecerebral blood flowcerebral oxygen deliveryhypoxianitric oxide

Identifiers

PMID26676248
PMCPMC4796739
OpenAlexW2209496750

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.