Evidence map›Paper›PMID 29436736›Full record

ArticleExperimental physiology2018

Psychological stress-induced cerebrovascular dysfunction: the role of metabolic syndrome and exercise.

Steven Brooks, Kayla W Branyan, Evan DeVallance, Roy Skinner, Kent Lemaster, J Whitney Sheets, Christopher R Pitzer, Shinichi Asano, Randall W Bryner, I Mark Olfert and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Experimental physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  9. Xanthine oxidase mediates chronic stress-induced cerebrovascular dysfunction and cognitive impairment.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Steven BrooksDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Kayla W BranyanDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Evan DeVallanceDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Roy SkinnerDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Kent LemasterDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
J Whitney SheetsDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Christopher R PitzerDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Shinichi AsanoDepartment of Health and Human Performance, Fairmont State University, WV, USA.
Randall W BrynerDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
I Mark OlfertDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.
Jefferson C FrisbeeDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
Paul D ChantlerDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, WV, USA.ORCID 0000-0001-6960-9728
West Virginia University · USWestern University · CAFairmont State University · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Laura F. Gibson · 2012 to 2026
$81.0M
West Virginia University Stroke COBREP20GM109098 · NIGMS · WEST VIRGINIA UNIVERSITY · PI HRUSKA, MARTIN · 2014 to 2024
$24.5M
American Heart Association-American Stroke Association 11CRP7370056American Heart Association-American Stroke Association 14PRE20380386NIGMS NIH HHS P20 GM109098NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

NEW

findingsWhat is the central question of this study? How does chronic stress impact cerebrovascular function and does metabolic syndrome accelerate the cerebrovascular adaptations to stress? What role does exercise training have in preventing cerebrovascular changes to stress and metabolic syndrome? What is the main finding and its importance? Stressful conditions lead to pathological adaptations of the cerebrovasculature via an oxidative nitric oxide pathway, and the presence of metabolic syndrome produces a greater susceptibility to stress-induced cerebrovascular dysfunction. The results also provide insight into the mechanisms that may contribute to the influence of stress and the role of exercise in preventing the negative actions of stress on cerebrovascular function and structure. ABSTRACT: Chronic unresolvable stress leads to the development of depression and cardiovascular disease. There is a high prevalence of depression with the metabolic syndrome (MetS), but to what extent the MetS concurrent with psychological stress affects cerebrovascular function is unknown. We investigated the differential effect of MetS on cerebrovascular structure/function in rats (16-17 weeks old) following 8 weeks of unpredictable chronic mild stress (UCMS) and whether exercise training could limit any cerebrovascular dysfunction. In healthy lean Zucker rats (LZR), UCMS decreased (28%, P < 0.05) ex vivo middle cerebral artery (MCA) endothelium-dependent dilatation (EDD), but changes in MCA remodelling and stiffness were not evident, though cerebral microvessel density (MVD) decreased (30%, P < 0.05). The presence of UCMS and MetS (obese Zucker rats; OZR) decreased MCA EDD (35%, P < 0.05) and dilatation to sodium nitroprusside (20%, P < 0.05), while MCA stiffness increased and cerebral MVD decreased (31%, P < 0.05), which were linked to reduced nitric oxide and increased oxidative levels. Aerobic exercise prevented UCMS impairments in MCA function and MVD in LZR, and partly restored MCA function, stiffness and MVD in OZR. Our data suggest that the benefits of exercise with UCMS were due to a reduction in oxidative stress and increased production of nitric oxide in the cerebral vessels. In conclusion, UCMS significantly impaired MCA structure and function, but the effects of UCMS were more substantial in OZR vs. LZR. Importantly, aerobic exercise when combined with UCMS prevented the MCA dysfunction through subtle shifts in nitric oxide and oxidative stress in the cerebral microvasculature.

Indexed as

AnimalsCardiovascular DiseasesDepressionEndothelium, VascularMaleMetabolic SyndromeMiddle Cerebral ArteryNitric OxideOxidative StressPhysical Conditioning, AnimalRatsRats, ZuckerStress, PsychologicalVasodilationNitric Oxidedepressionexercisemetabolic syndromestressvascular

Identifiers

PMID29436736
PMCPMC5927836
OpenAlexW2792467167

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.