Evidence map›Paper›PMID 24495184›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2014

Roles of Coagulation and fibrinolysis in angiotensin II-enhanced microvascular thrombosis.

Elena Y Senchenkova, Janice Russell, Charles T Esmon, D Neil Granger

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04338009 (The Randomized Elimination or Prolongation of Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Coronavirus Disease 2019), which is not on this map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.2field-weighted citation impact, top 21% 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.

NCT04338009 nacompletednot on this mapstarted 2020, after this paper: background citation

The Randomized Elimination or Prolongation of Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Coronavirus Disease 2019

TypeinterventionalSponsorUniversity of PennsylvaniaRan2020 to 2020Enrolled152ConditionsCOVID-19ArmsDiscontinuation of ARB/ACEI, Continuation of ARB/ACEI
3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 48 citations in OpenAlex.

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  16. Induced dysregulation of ACE2 by SARS-CoV-2 plays a key role in COVID-19 severity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
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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

4 authors at 3 institutions in 2 countries.

Elena Y SenchenkovaDepartment of Molecular & Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, USA; Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, Saint-Petersburg, Russia.
Janice Russell
Charles T Esmon
D Neil Granger
Louisiana State University Health Sciences Center Shreveport · USInstitute of Evolutionary Physiology and Biochemistry · RUOklahoma Medical Research Foundation · US

Funding

TRANSCAPILLARY FLUID EXCHANGER01HL026441 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI GRANGER, D. NEIL · 1985 to 2013
$4.0M
NHLBI NIH HHS HL26441-32NHLBI NIH HHS R01 HL026441
6 · The paper itself

Abstract

objectiveAngII-induced HTN is associated with accelerated thrombus development in arterioles. This study assessed the contributions of different components of the coagulation cascade and fibrinolysis to AngII-mediated microvascular thrombosis.

methodsLight/dye-induced thrombus formation (the time of onset and flow cessation) was quantified in cremaster muscle arterioles of AngII infused (two weeks) WT/AngII mice, EPCR-TgN, and mice deficient in PAI-1. WT/AngII mice were also treated with either tissue factor antibody, antithrombin III, heparin, hirudin, or murine APC.

resultsTF immunoblockade or hirudin treatment did not prevent the AngII-induced acceleration of thrombosis. While antithrombin III treatment prevented the acceleration in both thrombus onset and flow cessation, heparin only improved the time for blood flow cessation. Neither WT mice treated with murine APC nor EPCR-TgN were protected against AngII-induced thrombus development. A similar lack of protection was noted in PAI-1deficient mice.

conclusionThese findings implicate a role for thrombin generation pathway in the accelerated thrombosis induced by AngII and suggest that an impaired protein C pathway and increased PAI-1 do not make a significant contribution to this model of microvascular thrombosis.

Indexed as

Angiotensin IIAnimalsAntithrombin IIIAntithrombinsFibrinolysisHemostaticsMaleMiceMice, KnockoutMicrovesselsProtein CSerpin E2ThrombinThromboplastinThrombosisVasoconstrictor AgentsAngiotensin IIAntithrombin IIIAntithrombinsHemostaticsProtein CSerpin E2Serpine2 protein, mouseThrombinThromboplastinVasoconstrictor Agentsangiotensin IIanticoagulantscoagulationfibrinolysisthrombosis

Identifiers

PMID24495184
PMCPMC4107144
OpenAlexW2012833122

What OpenQuestion holds

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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 OpenQuestion graph.