Evidence map›Paper›PMID 10600857›Full record

ArticleThe American journal of physiology1999

Role of capillaries in determining CBF reserve: new insights using myocardial contrast echocardiography.

A R Jayaweera, K Wei, M Coggins, J P Bin, C Goodman, S Kaul

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in The American journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04575844 (Effects of Exercise and GLP-1 Agonism on Muscle Microvascular Perfusion and Insulin Action in Adults With Metabolic Syndrome), which is not on this map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
8.1field-weighted citation impact, top 2% 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.

NCT04575844 phase4recruitingstarted 2020, after this paper: background citation

Effects of Exercise and GLP-1 Agonism on Muscle Microvascular Perfusion and Insulin Action in Adults With Metabolic Syndrome

Ran2020Enrolled80Registered outcomes6Posted comparisons0ConditionsMetabolic SyndromeArmsExercise Training, liraglutide, Liraglutide + Exercise training
Open the trial in the graph
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 186 citations in OpenAlex.

  1. Trial
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  3. Effect of modest alcohol consumption over 1-2 weeks on the coronary microcirculation of normal subjects.European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology · 2010
    Trial
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  7. Review
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  14. Review
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  19. Diabetic Microvascular Disease: An Endocrine Society Scientific Statement.The Journal of clinical endocrinology and metabolism · 2017
    Review
  20. Coronary calcification compromises myocardial perfusion irrespective of luminal stenosis.International journal of cardiology. Heart & vasculature · 2017
    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

6 authors at 1 institution in 1 country.

A R JayaweeraCardiovascular Division, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.
K Wei
M Coggins
J P Bin
C Goodman
S Kaul
University of Virginia · US

Funding

ECHOCARDIOGRAPHIC ASSESSMENT OF MYOCARDIAL PERFUSIONR01HL048890 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI KAUL, SANJIV · 1992 to 2002
$1.0M
ECHOCARDIOGRAPHIC ASSESSMENT OF MICROVASCULAR PERFUSIONK08HL003909 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WEI, KEVIN S · 1999 to 2003
$507k
NHLBI NIH HHS K08-HL-03909NHLBI NIH HHS R01-HL-48890
6 · The paper itself

Abstract

To define the role of capillaries in the control of coronary blood flow (CBF) reserve, we developed a model of the coronary circulation and evaluated experimental data in its context. Our model comprised three compartments connected in series (arterial, capillary, and venous), each with its own resistance. The resistance in each vascular compartment was derived from the model based on hemodynamic data obtained in nine dogs during baseline and stenosis, both at rest and during hyperemia. The capillary hydrostatic pressure was assumed to be constant in all stages. Although in the absence of stenosis, the contribution of capillaries to total myocardial vascular resistance was only 25 +/- 5% at rest, it increased to 75 +/- 14% during hyperemia, despite the total myocardial vascular resistance decreasing by 51 +/- 13%. In the presence of a noncritical stenosis, total myocardial vascular resistance decreased by 22 +/- 10% at rest, with no change in capillary resistance. During hyperemia, total myocardial vascular resistance increased by 58 +/- 50% in the presence of the noncritical stenosis. In this situation, because arteriolar and venular resistances were already minimal, the increase in myocardial vascular resistance was due to increased capillary resistance, making it the predominant source (84 +/- 8%) of total myocardial vascular resistance. Myocardial video intensity (VI) on myocardial contrast echocardiography (MCE), which reflects capillary blood volume, decreased distal to the stenosis during hyperemia. In the presence of a flow-limiting stenosis at rest, myocardial VI also decreased, indicating that decrease in CBF was associated with an increase in capillary resistance. Our findings also provide an alternative explanation for the critical coronary closing pressure. Thus, contrary to previously held notions, capillaries play a vital role in the regulation of CBF.

Indexed as

Models, CardiovascularAnimalsArteriolesBlood PressureCapillariesCoronary CirculationCoronary DiseaseDogsEchocardiographyHeartHemodynamicsHomeostasisHydrostatic PressureMicrocirculationVascular ResistanceVenules

Identifiers

PMID10600857
OpenAlexW2162795567

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.