• Stanley Muravchick and Richard J Levy.
• Department of Anesthesiology and Critical Care, Hospital of the University of Pennsylvania, and The Children's Hospital of Philadelphia, 3400 Spruce Street, Philadelphia, PA 19104, USA. muravchst@uphs.upenn.edu
• Anesthesiology. 2006 Oct 1; 105 (4): 819-37.

AbstractMitochondria produce metabolic energy, serve as biosensors for oxidative stress, and eventually become effector organelles for cell death through apoptosis. The extent to which these manifold mitochondrial functions are altered by previously unrecognized actions of anesthetic agents seems to explain and link a wide variety of perioperative phenomena that are currently of interest to anesthesiologists from both a clinical and a scientific perspective. In addition, many surgical patients may be at increased perioperative risk because of inherited or acquired mitochondrial dysfunction leading to increased oxidative stress. This review summarizes the essential aspects of the bioenergetic process, presents current knowledge regarding the effects of anesthetics on mitochondrial function and the extent to which mitochondrial state determines anesthetic requirement and potential anesthetic toxicity, and considers some of the many implications that our knowledge of mitochondrial dysfunction poses for anesthetic management and perioperative medicine.

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