Abstract
Cardiac dysfunction is a well-known complication of severe sepsis and septic shock. Septic cardiomyopathy is characterized by reduced cardiac output and left ventricular pressures and biventricular dilatation, resulting in systemic hypoperfusion and multi-organ failure. There is emerging evidence suggesting that mediators of septic cardiomyopathy include cardio-depressive cytokines, Toll-like receptor signaling, cardiomyocyte production of reactive oxygen species and nitric oxide, and dysregulated Ca2+ homeostasis. This chapter will review the current evidence describing the cellular and molecular mechanisms of septic cardiomyopathy.
Keywords: Ca2+, Cardiomyocyte, Cecal ligation and puncture, Cytokines, Endotoxemia, Heart, Nitric oxide, Reactive oxygen species, Sepsis, Toll-like receptors.
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