Evidence map›Paper›PMID 28042109›Full record

ArticleAmerican journal of physiology. Renal physiology2017

A new mouse model of hemorrhagic shock-induced acute kidney injury.

Lei Wang, Jiangping Song, Jacentha Buggs, Jin Wei, Shaohui Wang, Jie Zhang, Gensheng Zhang, Yan Lu, Kay-Pong Yip, Ruisheng Liu

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 18 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

10 authors at 4 institutions in 2 countries.

Lei WangDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida; leiwang@health.usf.edu.
Jiangping SongDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Jacentha BuggsTampa General Hospital, Tampa, Florida.
Jin WeiDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Shaohui WangDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Jie ZhangDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Gensheng ZhangDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Yan LuDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi; and.
Kay-Pong YipDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Ruisheng LiuDepartment of Molecular Pharmacology & Physiology, University of South Florida College of Medicine, Tampa, Florida.
Florida College · USUniversity of South Florida · USTampa General Hospital · USUniversity of Mississippi Medical Center · US

Funding

Tubuloglomerular feedback and salt-sensitive hypertensionR01DK098582 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2013 to 2016
$1.3M
Primary cilia and modulation of the renal microcirculationR01DK099276 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2014 to 2017
$980k
NIDDK NIH HHS R01 DK098582NIDDK NIH HHS R01 DK099276
6 · The paper itself

Abstract

Current animal models of hemorrhagic shock-induced acute kidney injury (HS-induced AKI) require extensive surgical procedures and constant monitoring of hemodynamic parameters. Application of these HS-induced AKI models in mice to produce consistent kidney injury is challenging. In the present study, we developed a simple and highly reproducible mouse model of HS-induced AKI by combining moderate bleeding and renal pedicle clamping, which was abbreviated as HS-AKI. HS was induced by retroorbital bleeding of 0.4 ml blood in C57BL/6 mice. Mice were left in HS stage for 30 min, followed by renal pedicle clamping for 18 min at 36.8-37.0°C. Mean arterial pressure (MAP) and heart rate were monitored with preimplanted radio transmitters throughout the experiment. The acute response in renal blood flow (RBF) triggered by HS was measured with transonic flow probe. Mice received sham operation; bleeding alone and renal pedicle clamping alone served as respective controls. MAP was reduced from 77 ± 4 to 35 ± 3 mmHg after bleeding. RBF was reduced by 65% in the HS period. Plasma creatinine and kidney injury molecule-1 levels were increased by more than 22-fold 24 h after reperfusion. GFR was declined by 78% of baseline 3 days after reperfusion. Histological examination revealed a moderate-to-severe acute tubular damage, mostly at the cortex-medulla junction area, followed by the medullar and cortex regions. HS alone did not induce significant kidney injury, but synergistically enhanced pedicle clamping-induced AKI. This is a well-controlled, simple, and reliable mouse model of HS-AKI.

Indexed as

Disease Models, AnimalAcute Kidney InjuryAnimalsArterial PressureHepatitis A Virus Cellular Receptor 1Kidney Function TestsMaleMice, Inbred C57BLRenal CirculationReninReperfusion InjuryShock, HemorrhagicHavcr1 protein, mouseHepatitis A Virus Cellular Receptor 1Reninacute kidney injuryhemorrhagic shockmice

Identifiers

PMID28042109
PMCPMC5283893
OpenAlexW2552230216

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.