Abstract
The detailed mechanisms which cause heart failure have remained unclear. Previous studies demonstrated a correlation between oxidative stress markers and the severity of heart failure, indicating a crucial role of oxidative stress in the pathogenesis of heart failure. Superoxide appears to be one of the reactive oxygen species affecting oxidative stress in the heart. This oxygen-derived free radical is metabolized to hydrogen peroxide via superoxide dismutase (SDO), and hydrogen peroxide is subsequently detoxified into oxygen and water by catalase. It is important to note that superoxide is a precursor of many reactive oxygen species. Recent studies also documented a role of NADPH oxidase in oxidative stress in many organs including the heart. Oxidative stress produced by a relative increase in intracellular levels of superoxide is capable of inducing heart failure as well as cardiac dysfunction, resulting from hypertension, diabetes mellitus, obesity, inflammation and aging. Possible candidates for inhibitors toward cardiac oxidative stress in clinical practice are statins, angiotensin receptor antagonists and/or peroxisome proliferator-activated receptor agonists. However, it is still unclear whether anesthetics can regulate oxidative stress in the heart.
