BACKGROUND
Open heart surgery-associated ischemia/reperfusion (I/R) injury affects postoperative outcome, and a leading cause of this is lipid peroxidation. Congenital heart disease (CHD) patients, however, are less sensitive to I/R injury. Although little is known about the underlying molecular
BACKGROUND
Myocardial ischemia-reperfusion (I/R) results in the generation of oxygen-derived free radicals and the accumulation of lipid peroxidation-derived unsaturated aldehydes. However, the contribution of aldehydes to myocardial I/R injury has not been assessed.
OBJECTIVE
We tested the
The heart is a highly oxidative organ in which cardiomyocyte turnover is virtually absent, making it particularly vulnerable to accumulation of lipid peroxidation products (LPP) formed as a result of oxidative damage. Reactive oxygen and nitrogen species are the most common electrophiles formed
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