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Front Physiol. 2014 Sep 16;5:341. doi: 10.3389/fphys.2014.00341. eCollection 2014.

Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury.

Frontiers in physiology

Bhawana Agarwal, David F Stowe, Ranjan K Dash, Zeljko J Bosnjak, Amadou K S Camara

Affiliations

  1. Department of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA.
  2. Department of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA ; Department of Physiology, Medical College of Wisconsin Milwaukee, WI, USA ; Cardiovascular Research Center, Medical College of Wisconsin Milwaukee, WI, USA ; Zablocki VA Medical Center Milwaukee, WI, USA ; Department of Biomedical Engineering, Marquette University Milwaukee, WI, USA.
  3. Department of Physiology, Medical College of Wisconsin Milwaukee, WI, USA ; Department of Biomedical Engineering, Marquette University Milwaukee, WI, USA ; Biotechnology and Bioengineering Center, Medical College of Wisconsin Milwaukee, WI, USA.
  4. Department of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA ; Department of Physiology, Medical College of Wisconsin Milwaukee, WI, USA ; Cardiovascular Research Center, Medical College of Wisconsin Milwaukee, WI, USA.
  5. Department of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA ; Cardiovascular Research Center, Medical College of Wisconsin Milwaukee, WI, USA.

PMID: 25278902 PMCID: PMC4165278 DOI: 10.3389/fphys.2014.00341

Abstract

Mitochondria are critical modulators of cell function and are increasingly recognized as proximal sensors and effectors that ultimately determine the balance between cell survival and cell death. Volatile anesthetics (VA) are long known for their cardioprotective effects, as demonstrated by improved mitochondrial and cellular functions, and by reduced necrotic and apoptotic cell death during cardiac ischemia and reperfusion (IR) injury. The molecular mechanisms by which VA impart cardioprotection are still poorly understood. Because of the emerging role of mitochondria as therapeutic targets in diseases, including ischemic heart disease, it is important to know if VA-induced cytoprotective mechanisms are mediated at the mitochondrial level. In recent years, considerable evidence points to direct effects of VA on mitochondrial channel/transporter protein functions and electron transport chain (ETC) complexes as potential targets in mediating cardioprotection. This review furnishes an integrated overview of targets that VA impart on mitochondrial channels/transporters and ETC proteins that could provide a basis for cation regulation and homeostasis, mitochondrial bioenergetics, and reactive oxygen species (ROS) emission in redox signaling for cardiac cell protection during IR injury.

Keywords: cardiac IR injury; cardioprotection; electron transport chain; isoflurane; mitochondrial bioenergetics; volatile anesthetics

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