Evidence map›Paper›PMID 20175923›Full record

ArticleCritical care (London, England)2010

Renin-angiotensin system activation correlates with microvascular dysfunction in a prospective cohort study of clinical sepsis.

Kevin C Doerschug, Angela S Delsing, Gregory A Schmidt, Alix Ashare

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.0field-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

59 citing papers in PubMed, 122 citations in OpenAlex.

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  6. ATPflugers Archiv : European journal of physiology · 2025
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  19. Mechanisms of Post-critical Illness Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022
    Review
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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 1 institution in 1 country.

Kevin C DoerschugDepartment of Internal Medicine, University of Iowa Carver College of Medicine, 200 Hawkins Drive, Iowa City, Iowa, 52242, USA. kevin-doerschug@uiowa.edu
Angela S Delsing
Gregory A Schmidt
Alix Ashare
University of Iowa · US

Funding

UNIVERSITY OF IOWA CTSA FOR PEDIATRIC RESEARCHUL1RR024979 · NCRR · UNIVERSITY OF IOWA · PI ROSENTHAL, GARY E · 2007 to 2011
$31.8M
The role of microbial organisms in acute lung injuryK23HL071246 · NHLBI · UNIVERSITY OF IOWA · PI DOERSCHUG, KEVIN C · 2003 to 2007
$625k
The Organ Specific Role of Superoxide Dismutase in SepsisR03DK084057 · NIDDK · DARTMOUTH COLLEGE · PI ASHARE, ALIX · 2009 to 2010
$157k
NCRR NIH HHS UL1 RR024979NHLBI NIH HHS K23HL071246NIAAA NIH HHS K08DK073519-AANIAID NIH HHS L30 AI062287NIDDK NIH HHS R03 DK084057
6 · The paper itself

Abstract

introductionMicrovascular dysregulation characterized by hyporesponsive vessels and heterogeneous bloodflow is implicated in the pathogenesis of organ failure in sepsis. The renin-angiotensin system (RAS) affects the microvasculature, yet the relationships between RAS and organ injury in clinical sepsis remain unclear. We tested our hypothesis that systemic RAS mediators are associated with dysregulation of the microvasculature and with organ failure in clinical severe sepsis.

methodsWe studied 30 subjects with severe sepsis, and 10 healthy control subjects. Plasma was analyzed for plasma renin activity (PRA) and angiotensin II concentration (Ang II). Using near-infrared spectroscopy, we measured the rate of increase in the oxygen saturation of thenar microvascular hemoglobin after five minutes of induced forearm ischemia. In so doing, we assessed bulk microvascular hemoglobin influx to the tissue during reactive hyperemia. We studied all subjects 24 hours after the development of organ failure. We studied a subset of 12 subjects at an additional timepoint, eight hours after recognition of organ failure (early sepsis).

resultsAfter 24 hours of resuscitation to clinically-defined endpoints of preload and arterial pressure, Ang II and PRA were elevated in septic subjects and the degree of elevation correlated negatively with the rate of microvascular reoxygenation during reactive hyperemia. Early RAS mediators correlated with microvascular dysfunction. Early Ang II also correlated with the extent of organ failure realized during the first day of sepsis.

conclusionsRAS is activated in clinical severe sepsis. Systemic RAS mediators correlate with measures of microvascular dysregulation and with organ failure.

Indexed as

AdultAgedAged, 80 and overCase-Control StudiesFemaleHumansMaleMicrovesselsMiddle AgedProspective StudiesRenin-Angiotensin SystemSepsis

Identifiers

PMID20175923
PMCPMC2875539
OpenAlexW2134540051

What OpenQuestion holds

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LicenceCC BY
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.