Potential role of isoketals formed via the isoprostane pathway of lipid peroxidation in ischemic arrhythmias.

Boyden PA, Davies SS, Viswanathan PC, Amarnath V, Balser JR, Roberts LJ
J Cardiovasc Pharmacol. 2007 50 (5): 480-6

PMID: 18030056 · DOI:10.1097/FJC.0b013e31815a0564

Unabated reactive oxygen species (ROS) are potentiated by an ischemia-induced shift in anaerobic metabolism, which generates superoxide anion upon reperfusion and reintroduction of oxygen. ROS can modify protein structure and function in fundamental ways, one of which is by forming reactive lipid species from the oxidation of lipids. In this review, we discuss these pathways and discuss the literature that shows that these species can produce dramatic effects on cardiac ion channel function (eg, Na+ channel function). Furthermore, we review what is known about the generation of such in the highly remodeled post myocardial infarction substrate. We suggest prevention of adduction of these highly reactive compounds would be antiarrhythmic.

MeSH Terms (10)

Animals Arrhythmias, Cardiac F2-Isoprostanes Humans Lipid Peroxidation Molecular Structure Myocardial Ischemia Oxidative Stress Pyridoxamine Vitamin B Complex

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