It is well acknowledged that NO is critical in the pathogenesis of sepsis and that eNOS-mediated NO production is important in maintaining proper function of the cardiovascular system, while under pathological conditions (i.e., sepsis and ischemia reperfusion injury), deregulated or excessive release of NO by inducible NO synthase (iNOS) contributes substantially to cardiac dysfunction [26, 39]. This evidence concerns the gene NOS2 and ischemia reperfusion injury.