• Bruno B Peruchi, Fabrícia Petronilho, Hugo A Rojas, Larissa Constantino, Francielle Mina, Francieli Vuolo, Mariane R Cardoso, Cinara L Gonçalves, Gislaine T Rezin, Emílio L Streck, and Felipe Dal-Pizzol.
• Laboratório de Fisiopatologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
• J. Surg. Res. 2011 May 15;167(2):e333-8.

BackgroundThe derangement in oxygen utilization occurring during sepsis is likely to be linked to impaired mitochondrial functioning. Skeletal muscle comprises 50%-60% of body cell mass and represents the largest organ potentially affected by systemic inflammation. Thus, we investigated whether sepsis induced by cecal ligation and puncture (CLP) modifies mitochondrial activity in respiratory and nonrespiratory skeletal muscle.Materials And MethodsWistar rats were subjected to CLP and at different times, diaphragm and quadriceps were removed for the determination of electron transfer chain activities and mitochondrial oxidative stress. In addition, we determined diaphragm contractile strength.ResultsIn the quadriceps, 12 h after CLP we demonstrated a significant diminution on complex II-III activity. At late times (48 h after CLP), we demonstrated a decrease in the activity of all electron transfer chain complexes, which seemed to be secondary to early oxidative stress and correlates with diaphragm contractile strength. Differently from diaphragm, electron transfer chain was not decreased after sepsis and even oxidative stress was not increased at all times tested.ConclusionOur results suggest that quadriceps mitochondria are more resistant to sepsis-induced dysfunction.Copyright © 2011 Elsevier Inc. All rights reserved.

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