Several cellular and molecular mechanisms have been implicated in the development of
myocardial dysfunction and low cardiac output in pediatric patients undergoing heart surgery. Ischemia-
reperfusion injury with alterations in calcium homeostasis as well as mitochondrial function has
been strongly related to myocyte damage and heart failure in this population. In this article, we will review
the main mechanisms of postoperative cardiac dysfunction at cellular and molecular levels and the subsequent protective
strategies. In addition, we will describe cellular features of the neonatal or immature myocardium and will suggest
possible protective management strategies. This article addresses the first of eight topics comprising the special issue entitled
“Pharmacologic strategies with afterload reduction in low cardiac output syndrome after pediatric cardiac surgery”.
Keywords: Cardiac surgery, ischemia-reperfusion injury, mitochondria, auto transplantation, cyanosis, ventricular hypertrophy.
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