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.
Highlights
In recent years the mitochondrion has gained recognition as a key factor in the etiology of numerous diseases (Duchen, 2004), including cardiac ischemia and reperfusion (IR) injury (Ferrari, 1996; Murphy and Steenbergen, 2008b)
Cardiac IR-induced mitochondrial dysfunction is accompanied by reduced membrane potential ( m), decreased adenosine triphosphate (ATP) production, impaired Ca2+ homeostasis, increased “bad” reactive oxygen species (ROS) emission, matrix swelling and membrane permeability, and release of cytochrome c and other apoptotic factors leading to cell death (Steenbergen et al, 1990; Stowe and Camara, 2009) (Figure 1)
The study proposed that differences in the mitochondrial genome modulate isoflurane-induced generation of ROS that translates into a differential susceptibility to APC; this suggested a potentially important role of mitochondrial DNA (mDNA) in regulating cardioprotection in APC via modulation of ROS production
Summary
In recent years the mitochondrion has gained recognition as a key factor in the etiology of numerous diseases (Duchen, 2004), including cardiac ischemia and reperfusion (IR) injury (Ferrari, 1996; Murphy and Steenbergen, 2008b). Cardioprotective strategies include a complex cascade of signaling events (Zaugg and Schaub, 2003) that involve the electron transport chain (ETC) and key factors in the intrinsic anti-apoptotic signaling pathways that lead to cell protection. Cardiac IR-induced mitochondrial dysfunction is accompanied by reduced membrane potential ( m), decreased adenosine triphosphate (ATP) production, impaired Ca2+ homeostasis, increased “bad” reactive oxygen species (ROS) emission, matrix swelling and membrane permeability, and release of cytochrome c and other apoptotic factors leading to cell death (Steenbergen et al, 1990; Stowe and Camara, 2009) (Figure 1). Pre- and postconditioning by volatile anesthetics (VA) have emerged as useful strategies to protect the myocardium against IR injury (Zaugg et al, 2003b; Pagel, 2008; Hu and Liu, 2009; Camara et al, 2010). The guidelines of the American College of Cardiology and the American Heart Association recommend the maintenance of VA for non-cardiac surgery in patients with increased risk www.frontiersin.org
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