Evidence map›Paper›PMID 26702145›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Increased peripheral vascular disease risk progressively constrains perfusion adaptability in the skeletal muscle microcirculation.

Jefferson C Frisbee, Joshua T Butcher, Stephanie J Frisbee, I Mark Olfert, Paul D Chantler, Lawrence E Tabone, Alexandre C d'Audiffret, Carl D Shrader, Adam G Goodwill, Phoebe A Stapleton and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Protection from vascular dysfunction in female rats with chronic stress and depressive symptoms.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Cardiovascular consequences of metabolic syndrome.Translational research : the journal of laboratory and clinical medicine · 2017
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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

13 authors at 2 institutions in 1 country.

Jefferson C FrisbeeDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Basic and Translational Stroke Research, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and jefrisbee@hsc.wvu.edu.
Joshua T ButcherDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Stephanie J FrisbeeDepartment of Health Policy, Management and Leadership, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Basic and Translational Stroke Research, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
I Mark OlfertDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Paul D ChantlerDivision of Exercise Physiology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Basic and Translational Stroke Research, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Lawrence E TaboneDepartment of Surgery, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Alexandre C d'AudiffretDepartment of Surgery, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Carl D ShraderDepartment of Family Medicine, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Adam G GoodwillDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Phoebe A StapletonDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Steven D BrooksDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Robert W BrockDepartment of Physiology and Pharmacology, West Virginia University Health Sciences Center, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, West Virginia University Health Sciences Center, Morgantown, West Virginia; and.
Julian H LombardDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
West Virginia University · USMedical College of Wisconsin · US

Funding

WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
West Virginia University Stroke COBREP20GM109098 · NIGMS · WEST VIRGINIA UNIVERSITY · PI HRUSKA, MARTIN · 2014 to 2024
$24.5M
HIGH SALT DIET, ANGIOTENSIN II, AND MICROVESSEL DILATIONR01HL065289 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LOMBARD, JULIAN H · 2000 to 2012
$3.8M
Skeletal Muscle Microcirculation in Obese Zucker RatsR01DK064668 · NIDDK · WEST VIRGINIA UNIVERSITY · PI FRISBEE, JEFFERSON C · 2004 to 2009
$1.1M
MECHANISM OF VASCULAR OXYGEN RESPONSE IN HYPERTENSIONR01HL037374 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LOMBARD, JULIAN H · 1987 to 2000
$142k
NCRR NIH HHS P20 RR-016477NHLBI NIH HHS R01 HL-065289NHLBI NIH HHS R01 HL-37374NIAMS NIH HHS RR-2865ARNIDDK NIH HHS R01 DK-64668NIGMS NIH HHS 1P20 GM-109098
6 · The paper itself

Abstract

To determine the impact of progressive elevations in peripheral vascular disease (PVD) risk on microvascular function, we utilized eight rat models spanning "healthy" to "high PVD risk" and used a multiscale approach to interrogate microvascular function and outcomes: healthy: Sprague-Dawley rats (SDR) and lean Zucker rats (LZR); mild risk: SDR on high-salt diet (HSD) and SDR on high-fructose diet (HFD); moderate risk: reduced renal mass-hypertensive rats (RRM) and spontaneously hypertensive rats (SHR); high risk: obese Zucker rats (OZR) and Dahl salt-sensitive rats (DSS). Vascular reactivity and biochemical analyses demonstrated that even mild elevations in PVD risk severely attenuated nitric oxide (NO) bioavailability and caused progressive shifts in arachidonic acid metabolism, increasing thromboxane A2 levels. With the introduction of hypertension, arteriolar myogenic activation and adrenergic constriction were increased. However, while functional hyperemia and fatigue resistance of in situ skeletal muscle were not impacted with mild or moderate PVD risk, blood oxygen handling suggested an increasingly heterogeneous perfusion within resting and contracting skeletal muscle. Analysis of in situ networks demonstrated an increasingly stable and heterogeneous distribution of perfusion at arteriolar bifurcations with elevated PVD risk, a phenomenon that was manifested first in the distal microcirculation and evolved proximally with increasing risk. The increased perfusion distribution heterogeneity and loss of flexibility throughout the microvascular network, the result of the combined effects on NO bioavailability, arachidonic acid metabolism, myogenic activation, and adrenergic constriction, may represent the most accurate predictor of the skeletal muscle microvasculopathy and poor health outcomes associated with chronic elevations in PVD risk.

Indexed as

MicrocirculationAnimalsArteriolesFructoseHypertension, RenalMuscle, SkeletalNitric OxideOxygen ConsumptionPerfusionPeripheral Vascular DiseasesRatsRats, Inbred DahlRats, Inbred SHRRats, Sprague-DawleyRats, ZuckerRisk AssessmentFructoseNitric OxideSodium, DietaryThromboxane A2blood flow regulationmicrovascular dysfunctionperipheral vascular diseaserodent models of cardiovascular disease risksystem biology of microcirculation

Identifiers

PMID26702145
PMCPMC4796615
OpenAlexW2323724643

What Socratic 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 Socratic graph.