Abstract
The pathways for the metabolism of molecular oxygen involve one electron-transfer reaction with the subsequent production of reduced-oxygen intermediates. These reduced-oxygen intermediates include the superoxide anion (·O -2 ), hydrogen peroxide (H2O2), and the hydroxyl radical (·OH), which are highly reactive, short-lived species. Normally, intracellular enzyme systems that include superoxide dismutase, catalase, and glutathione peroxidase are responsible for “scavenging” these products of oxygen metabolism. However, in many pathological states such as inflammation, ischemia, and reperfusion, there is an increased production of these reduced-oxygen intermediates, which are capable of extensive tissue damage. It is the purpose of this symposium to examine, in depth, the role of oxygen free radical systems as mediators of myocardial dysfunction and expand our knowledge of myocardial ischemia, ischemia—reperfusion injury, and the inflammatory response of the myocardium.
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Hess, M.L., Manson, N.H. (1985). The Oxygen Free Radical System and Myocardial Dysfunction. In: Harris, P., Poole-Wilson, P.A. (eds) Advances in Myocardiology. Advances in Myocardiology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1287-2_13
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DOI: https://doi.org/10.1007/978-1-4757-1287-2_13
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