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Hepatic Ischemia/Reperfusion Injury Is Diminished by Atorvastatin in Wistar Rats

  • Carlos Rodrigo Cámara-Lemarroy
    ,
  • Francisco Javier Guzmán-de la Garza
    ,
  • ,
  • Paula Cordero-Pérez
    ,
  • Linda Muñoz-Espinosa
    ,
  • Liliana Torres-González
  • Hospital Universitario Dr. Jose Eleuterio Gonzalez
Research Output:
Contribution to journal
Article
Peer-review

Publication metrics

Metrics

SciVal
Citations
18
SciVal
FWCI
1.81
SciVal
Author count
7
SciVal
Paper percentile
85
Scopus
Citations

Abstract

Background and Aims: Temporal occlusion of the hepatoduodenal ligament (HDL) is often used during liver surgeries in order to reduce blood loss, resulting in ischemia/reperfusion injury (I/R). The aim of the study was to investigate the effects of atorvastatin (ATOR) on hepatic I/R injury and on serum levels of tumor necrosis factor-alpha (TNF-α), endothelin-1 (ET-1), antithrombin III (ATIII) and intracellular adhesion molecule-1 (ICAM-1). Methods: Liver ischemia was induced in Wistar rats by clamping the HDL for 60 min, followed by either 60 or 180 min reperfusion. Rats received either vehicle or 10 mg/kg ATOR before hepatic I/R. Control group received sham surgery. Livers were examined for histological damage and serum AST, ALT, TNF-α, ET-1, ATIII and ICAM-1 concentrations were measured. Results: After I/R, AST and ALT were significantly elevated, ATIII levels were significantly depleted, both TNF-α and ICAM-1 levels increased and ET-1 was significantly elevated (at 180 min). ATOR pretreatment attenuated these alterations and diminished histological injury scores. Conclusions: Our results show that ATOR protects the liver from I/R injury.

Publication Information

Output type

Research Output:
Contribution to journal
Article
Peer-review

Original language

English

Pages from-to (Number of pages)

Pages 210-216 (7 pages)

Journal (Volume, Issue Number)

Archives of Medical Research (Volume 45, Issue 3)

Publication milestones

  • Published - 04/2014

Publication status

Published - 04/2014

ISSN

0188-4409

Publication IDs

  • Scopus: 84899543720
  • WOS: 000336011600003