Oxidative stress precedes skeletal muscle mitochondrial dysfunction during experimental aortic cross-clamping but is not associated with early lung, heart, brain, liver, or kidney mitochondrial impairment.

Date publication

octobre 2014

Journal

Journal of vascular surgery

Auteurs

Membres identifiés du Cancéropôle Est :
Dr CHAMARAUX-TRAN Thiên-Nga , Pr GENY Bernard , Dr ZOLL Joffrey

Tous les auteurs :
Guillot M, Charles AL, Chamaraux-Tran TN, Bouitbir J, Meyer A, Zoll J, Schneider F, Geny B

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/24095040

Résumé

Lower limb ischemia-reperfusion results in skeletal muscle mitochondrial alterations, production of reactive oxygen species (ROS), and remote organ impairments that are largely involved in patient prognosis. However, whether ischemia without reperfusion increases ROS production and precedes mitochondrial alteration and whether mitochondrial dysfunction occurs early in remote organs is unknown. This study determined muscle mitochondrial function and ROS production after ischemia alone, or followed by two periods of reperfusion, and investigated heart, lung, liver, kidney, and brain mitochondrial functions after lower limb ischemia-reperfusion.

Mots clés

Animals, Aorta, Abdominal, surgery, Disease Models, Animal, Immunohistochemistry, Ischemic Preconditioning, Kidney, metabolism, Liver, metabolism, Lower Extremity, blood supply, Lung, metabolism, Male, Mitochondria, metabolism, Mitochondria, Heart, metabolism, Mitochondria, Liver, metabolism, Mitochondrial Diseases, etiology, Oxidative Stress, physiology, Rats, Rats, Wistar, Reactive Oxygen Species, metabolism, Reperfusion Injury, metabolism

Référence

J. Vasc. Surg.. 2014 Oct;60(4):1043-51.e5