Background and Aims A progressive ventricular dysfunction caused by ischemic myocardial injuries remains one of the leading causes of death during the postoperative course in congenital heart disease (CHD). The aim of this study was to investigate the role of oxidative stress in these myocardial injuries.
Methods Myocardial injuries and oxidative stress mechanisms were assessed by histopathology and immunohistochemistry and quantified by morphometrical analyses.
Results Myocardial injury was observed in pediatric patients submitted to surgery for CHD with cardiopulmonary bypass, followed by lethal exit. Oxidative stress mechanisms were directly related to these particular types of myocardial injuries. Importantly, 4- hydroxinonenal (4-HNE), a marker of lipid peroxidation, is strongly expressed, especially in irreversible myocardial lesions. Although morphologically similar, myocardial injuries observed in patients who evolved with sepsis in the peri-operatory period exhibited a completely different set of oxidative stress mechanisms. Increased concentrations of nitrotyrosine protein adducts were observed in these patients, suggesting that peroxynitrite-mediated protein nitration may be the predominant oxidative stress mechanism found in these situations.
Conclusions The underlying mechanisms of these lesions seem to be related to the development of ischemia or ischemia/reperfusion followed by oxidative stress mechanisms that vary depending on whether sepsis was present. While the exact mechanism is not fully understood, it has been suggested that endogenous catecholamine release could have a role in this process.
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