Evidence map›Paper›PMID 22923620›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Autoregulation and mechanotransduction control the arteriolar response to small changes in hematocrit.

Krishna Sriram, Beatriz Y Salazar Vázquez, Amy G Tsai, Pedro Cabrales, Marcos Intaglietta, Daniel M Tartakovsky

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 37 citations in OpenAlex.

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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

6 authors at 1 institution in 2 countries.

Krishna SriramDepartment of Mechanical and Aerospace Engineering, University of California-San Diego, La Jolla, California 92093-0412, USA.
Beatriz Y Salazar Vázquez
Amy G Tsai
Pedro Cabrales
Marcos Intaglietta
Daniel M Tartakovsky
University of California, San Diego · US

Funding

BIOENGINEERING DESIGN OF ARTIFICIAL BLOODR24HL064395 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI INTAGLIETTA, MARCOS · 2000 to 2004
$5.0M
TRANSFUSION TRIGGER EXTENSION BY PLASMA EXPANDERSR01HL062354 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI INTAGLIETTA, MARCOS · 2000 to 2009
$2.9M
Plasma hyperviscosity for the reversal of hypovolemic cardiovascular collapseR01HL076182 · NHLBI · LA JOLLA BIOENGINEERING INSTITUTE · PI TSAI, AMY G · 2004 to 2007
$1.8M
NHLBI NIH HHS R01-HL-062354NHLBI NIH HHS R01-HL-076182NHLBI NIH HHS R24-HL-064395
6 · The paper itself

Abstract

Here, we present an analytic model of arteriolar mechanics that accounts for key autoregulation mechanisms, including the myogenic response and the vasodilatory effects of nitric oxide (NO) in the vasculature. It couples the fluid mechanics of blood flow in arterioles with solid mechanics of the vessel wall and includes the effects of wall shear stress- and stretch-induced endothelial NO production. The model can be used to describe the regulation of blood flow and NO transport under small changes in hematocrit and to analyze the regulatory response of arterioles to small changes in hematocrit. Our analysis revealed that the experimentally observed paradoxical increase in cardiac output with small increases in hematocrit results from the combination of increased NO production and the effects of a strong myogenic response modulated by elevated levels of WSS. Our findings support the hypothesis that vascular resistance varies inversely with blood viscosity for small changes in hematocrit in a healthy circulation that responds to shear stress stimuli. They also suggest beneficial effects independent of changes in O(2) carrying capacity associated with the postsurgical transfusion of one or two units of blood.

Indexed as

Computer SimulationHematocritModels, TheoreticalArteriolesBlood ViscosityCardiac OutputHomeostasisHumansMechanotransduction, CellularModels, CardiovascularNitric OxideRegional Blood FlowStress, MechanicalVascular ResistanceVasodilationNitric Oxide

Identifiers

PMID22923620
PMCPMC3517642
OpenAlexW2097339703

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.