Evidence map›Paper›PMID 20363892›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Akt1 genetic deficiency limits hypothermia cardioprotection following murine cardiac arrest.

David G Beiser, Kimberly R Wojcik, Danhong Zhao, Gerasim A Orbelyan, Kimm J Hamann, Terry L Vanden Hoek

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. CPR: cardiac phosphatase in resuscitation.The Journal of clinical investigation · 2023
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  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Optimal protective hypothermia in arrested mammalian hearts.Therapeutic hypothermia and temperature management · 2015
    Article
  11. Article
  12. Article
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  15. Article
  16. Article
  17. 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

6 authors at 2 institutions in 2 countries.

David G BeiserSect. of Emergency Medicine, 5841 S. Maryland Ave., MC 5068, Chicago, IL 60637, USA. dbeiser@uchicago.edu
Kimberly R Wojcik
Danhong Zhao
Gerasim A Orbelyan
Kimm J Hamann
Terry L Vanden Hoek
Resuscitation Council · GBUniversity of Chicago · US

Funding

Preconditioning against a source of reperfusion oxidantsR01HL068951 · NHLBI · UNIVERSITY OF CHICAGO · PI VANDEN HOEK, TERRY L. · 2002 to 2006
$1.9M
Oxidants &Caspases: Initiation of Reperfusion InjuryR01HL079641 · NHLBI · UNIVERSITY OF CHICAGO · PI HAMANN, KIMM J · 2005 to 2009
$1.8M
Mechanisms of Hypothermic Protection from Ischemia/Reperfusion Cardiac InjuryR01HL084643 · NHLBI · UNIVERSITY OF CHICAGO · PI HAMANN, KIMM J · 2007 to 2010
$1.5M
Hypothermia for Cardiac Arrest: Optimizing Akt-Nitric Oxide Synthase SignalingK08HL091184 · NHLBI · UNIVERSITY OF CHICAGO · PI BEISER, DAVID GUSTAV · 2008 to 2012
$621k
NHLBI NIH HHS K08 HL091184NHLBI NIH HHS K08-HL-091184NHLBI NIH HHS R01-HL-68951NHLBI NIH HHS R01-HL-79641NHLBI NIH HHS R01-HL-84643
6 · The paper itself

Abstract

Therapeutic hypothermia (TH) cardioprotection has recently been associated with increased Akt signaling in a rat model of cardiac arrest. However, it is not known whether Akt is required for this beneficial effect of TH. We used a mouse model of cardiac arrest demonstrating TH cardioprotection to study the response of mice deficient in an Akt1 allele. We hypothesized that Akt1 mediates TH cardioprotection and that decreases in Akt1 content would diminish such protection. Adult C57BL/6 wild-type (WT) mice underwent an 8-min cardiac arrest. After 6 min, the mice were randomized to normothermia (WT(NT), 37 degrees C) or TH (WT(TH), 30 degrees C). Following cardiopulmonary resuscitation and the return of spontaneous circulation (ROSC), the animals were hemodynamically monitored for 240 min (R240). At R240, cardiac tissue Akt content and phosphorylation were assayed. Studies were repeated in Akt1 heterozygous (Akt1(+/-)) mice. As a result, baseline characteristics and ROSC rates were equivalent across groups. At R240, WT(TH) mice exhibited lower heart rate, larger stroke volume, and higher cardiac output than WT(NT) animals (P < 0.05). Cardioprotection in WT(TH) at R240 was associated with increased cardiac Akt phosphorylation at Ser473 and Thr308 compared with that in WT(NT) (P < 0.05). TH-associated alterations in Akt phosphorylation, stroke volume, heart rate, and cardiac output were abrogated in Akt1(+/-) animals. In conclusion, TH improves post-ROSC cardiac function and increases Akt phosphorylation in WT, but not Akt1(+/-), mice. The Akt1 isoform appears necessary for TH-mediated cardioprotection.

Indexed as

AnimalsCardiac OutputFemaleHeart ArrestHemodynamicsHypothermia, InducedMiceMice, Inbred C57BLModels, AnimalPhosphorylationProto-Oncogene Proteins c-aktStroke VolumeAkt1 protein, mouseProto-Oncogene Proteins c-akt

Identifiers

PMID20363892
PMCPMC2886630
OpenAlexW2138917937

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.